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Dietary intakes and leptin concentration

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Leptin, a peptide contained 146 amino-acids, is mostly secreted from adipose tissue and it has a critical role on regulation of body weight, body fat mass, appetite, and food intakes. We tried to review the previous evidence regarding the effects of dietary intakes, including consumption of carbohydrates, fats and protein on concentrations of leptin concentration. We searched in PubMed search engine to January 2013 by using the following key words: dietary intake, diet, dietary fat, high-fat diet, dietary carbohydrate, high carbohydrate diet, dietary protein, high protein diet in combination with leptin, adipokine. Then, we recruited 35 articles to review in the present study. It seems that beside the amount of fats, type of fatty acids have the key roles on circulating leptin concentration. Energy intake also significantly associated with the hormone. Studies regarding the association between carbohydrate intake and concentration of lepton have been reached to contradictory results. It seems that protein intake can increase the lepton activity. Findings from several studies suggest that a diet display an important role on change the concentration of lepton.
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1- Food Security Research Center AND Department of Community Nutrition, School of Nutrition and Food Science, Isfahan University
of Medical Sciences, Isfahan, Iran
Correspondence to: Leila Azadbakht, Email: azadbakht@hlth.mui.ac.ir
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Dietary intakes and leptin concentrations
Vajiheh Izadi
(1)
, Sahar Saraf-Bank
(1)
, Leila Azadbakht
(1)
Abstract
BACKGROUND:
Leptin, a peptide contained 146 amino-acids, is mostly secreted from adipose tissue
and it has a critical role on regulation of body weight, body fat mass, appetite, and food intakes. We
tried to review the previous evidence regarding the effects of dietary intakes, including consumption
of carbohydrates, fats and protein on concentrations of leptin concentration.
METHODS:
We searched in PubMed search engine to January 2013 by using the following key
words: dietary intake, diet, dietary fat, high-fat diet, dietary carbohydrate, high carbohydrate
diet, dietary protein, high protein diet in combination with leptin, adipokine. Then, we recruited
35 articles to review in the present study.
RESULTS:
It seems that beside the amount of fats, type of fatty acids have the key roles on circulating
leptin concentration. Energy intake also significantly associated with the hormone. Studies regarding
the association between carbohydrate intake and concentration of lepton have been reached to
contradictory results. It seems that protein intake can increase the lepton activity.
CONCLUSION:
Findings from several studies suggest that a diet display an important role on
change the concentration of lepton.
Keywords: Diet, Carbohydrate, Protein, Fat, Leptin
Date of submission:
16 Jun 2013,
Date of acceptance:
9 Oct 2013
Introduction
Leptin, a 16 kDa protein, is a peptide contained 146
amino-acids that are discovered in 1994. Leptin is
mostly secreted from adipose tissue, and it has a
critical role on regulation of body weight and also
body fat mass.
1-3
It markedly regulates energy
expenditure, appetite, thermogenesis and food
intakes. Leptin caused to increase fatty acids
oxidation and decrease triglyceride synthesis and so
that it attenuates lipogenic action of insulin and
increases insulin sensitivity of muscle and liver. This
hormone has the favorable effect on glucose
homeostasis.
4-7
Given the key role of leptin on
regulation of body weight and prevention of obesity,
it seemed that leptin levels were decreased during the
elevation of body weight.
8
But according to a large
body of evidence, most obese humans have higher
circulations of leptin.
9
It has been indicated that
obesity might induces state of leptin resistance.
10
Inactivation of leptin receptors enhance leptin
resistance and reduces satiety, and it enhances the
risk of obesity.
5
Therefore, treatment of obesity tends
to increase leptin action in central nervous system
(CNS), which is able to decrease food intake and
body fat through the reduction of energy intakes.
1,5,8
Expression and secretion of leptin is enhanced
by estrogen, tumor necrosis factor-α, corticosteroids
as well as glucose and insulin. In contrast, T
4
,
growth hormone, catecholamine, androgens and
free fatty acids suppress the expression of this
hormone.
11,12
Among these parameters, diet-related
factors display the important roles on augmentation
and amelioration of this hormone.
13-19
Among diet-related factors, dietary components
including consumption of beverages, fatty acids,
proteins and carbohydrates have been shown to
have a significant association with concentrations of
leptin.
1,15,20-22
However, contradictory results are
found in this regard. Based on several evidence diets
rich in polyunsaturated fatty acids (PUFA) (ɷ
3
and
ɷ
6
) leads to increase circulating of leptin compared
to diet rich in monounsaturated fatty acids (MUFA)
and saturated fatty acids (SFA),
20
In contrast,
according to some studies consumption of ɷ
3
fatty
acids showed a reduction in leptin gene
expression.
23,24
High carbohydrate diet might
Review Article
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increase leptin sensitivity in some studies.
5,8
Beside
percent consumption of carbohydrate, glycemic
index and glycemic load of carbohydrate also have
been indicated to have a critical role on
concentrations of leptin.
16
In this review article, we tried to review the
previous evidence regarding the effects of dietary
intakes, including consumption of carbohydrates,
fats and protein on concentrations of leptin and also
explain about potential underlying mechanism in
this regard.
Materials and Methods
To investigate the relationship between dietary
intakes and concentrations of leptin, we searched in
PubMed search engine from 2000 to January 2013
using the following key words to the topics: dietary
intake, diet, dietary fat, high fat diet, dietary
carbohydrate, high carbohydrate diet, dietary
protein, high protein diet in combination with
leptin, adipokine. All 265 articles with design of
clinical trial, cohort and cross-sectional studies have
been reviewed. 35 articles were recruited in this
study, and others were excluded owing to lack of
the direct relation with this issue, duplication and
lack of full-text articles. Studies that investigated
among association between dietary intakes and
leptin concentrations are shown in table 1.
Table 1. Studies regarding the association between dietary intakes and concentrations of leptin
Study
Type of
study
Numbers/sex Age (year)/BMI Design and aim
Duration of
study
Results
1 Parallel
55 obese men and
women
Age: 25.7 ± 5.4
Effect of diets with 3 types
of fat (olive, rapeseeds,
sunflower oil)
2 weeks diet with
SFA and 4
intervention diets
Serum levels of
leptin effect on diet
rich in α-linoleic
acids
BMI: 23.0 ± 2.3
6 Parallel
18 women and
men
Age: 45.3 ± 13.6
Effect of high carbohydrate
low fat on serum level of
leptin (35% fat, 45% CHO,
20% protein) compared to
(15% fat, 65% CHO, 20%
protein)
2 weeks weight
maintenance, 2
weeks isocaleric
and 12 weeks
weight loss diet
No change was
found in level of
leptin and increase
in leptin sensitivity
BMI: 27.1 ± 2.3
8
Cross
sectional
31 (women and
men) cirrhosis
patients and 10
controls
Age: 54-57
Assessing the association
between energy intakes
and leptin
-
No significant
relationship was
found
BMI: 25.7-56.5
9 Parallel
19 lean and obese
women
Age: 21.5 ± 1.9
Isocaleric meals: 166 g
CHO, 38 g protein and 70
g fat, 36 g protein
-
Significant lower
levels of leptin after
carbohydrate meals
in obese women
compared to lean
women
BMI: 21.6 ± 1.8
Age: 34.6 ± 7.8
BMI: 49.8 ± 6.9
16 Parallel
19 women and
men
Age: 41 ± 11
Effect of high protein diet
on leptin (50% CHO, 35%
fat, 15% protein) compared
to (50% CHO, 20% fat,
30% protein)
2 weeks normal
diet with weight
maintenance 2
weeks isocarelie
high protein diet,
12 weeks high
protein weight
loss diet
Greater status of
satiety with no
change in plasma
leptin after high
protein diet
BMI: 26.2 ± 2.1
17
Cross
sectional
165 healthy
overweight and
obese women in
postmenauposal
status
Age: 60.73 ± 6.7
Assessing the association
between habitual dietary
intakes and leptin
-
Inverse relationship
between
consumption of high
carbohydrate and fat
with hormone
BMI: 30.5 ± 3.9
18 Parallel
13 lean and
overweight men
Age: 18-27
High carbohydrate, low fat
meals (80% CHO, 17%
protein, 3% fat)
3 days
No significant
difference was
found
BMI: 20.8 ± 0.7
30.8 ± 1.7
19 Parallel 200 women
Age: 100 women with 50
100 women: > 50
Diet rich in fruits,
vegetables and fiber with
low amount of fat
12 months
Had no effect on
leptin
BMI: 25.7
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Table 1. Studies regarding the association between dietary intakes and concentrations of leptin (Continue)
Study
Type of
study
Numbers/sex Age (year)/BMI
Design and aim
Duration
of study
Results
20
Cross
sectional
60 men and
women with
Type 1 diabetese
Age: 22.8 ± 6.8
Assessing the association
between consumption of
SFA and PUFA and lepton
-
Positive relationship with
consumption of SFA and
lepton in men/ positive and
negative association
between linolenic acid and
arashidonic acids and
leptin, respectively
BMI: 22.7 ± 2.3
25 Experimental
344 female rats
-
High fat diet in comparison
with low fat with complex
carbohydrate
20 months
Increase in plasma level of
hormone by the high fat
diet
26 Cross over
9 men and
women
Age: 20-37
High carbohydrate diet with
different in glycemic index
and fat in 4 groups
8 days
17% greater in diets with
high glycemic index
BMI: 18-26
27 Experimental
rats -
Effect of type of fat in low
calorie diet on leptin
10 weeks
60% increase in leptin
concentration among fish
oil and sunflower oil fed
compared to beef tallow fed
28
Cross
sectional
211 male and
205 female of
Japanese-
American in
Hawaii and
Japanese in
Japan
Age: 40-59
Assessing the association
between energy intake and
serum leptin concentration
-
Inverse relationship
between energy intake and
serum level of leptin in
obese persons
BMI: < 25 and 25
29 Parallel 44 healthy male
Age: 43 ± 5
Effect of low calorie diet on
plasma leptin
4 days
39.4% decrease in leptin by
the energy restricted diet BMI: 27.3 ± 3.2
BMI: Body mass index; PUFA: Polyunsaturated fatty acid; SFA: Saturated fatty acid; CHO: Carbohydrate
Results
Carbohydrate intake and concentrations of leptin:
results from studies evaluated the association
between adherence to high carbohydrate diet and
leptin concentration have been shown to reach
contradictory results.
5,6,16,17,30
Consumption of carbohydrate with high
glycemic load may leads to leptin resistance.
6,17
However, consumption of the high amount of fiber
and high carbohydrate diet were found to have a
decreased concentration of leptin and increase in
insulin sensitivity, respectively.
5,8,16
One crossover
clinical trial study conducted among 9 healthy
individuals indicated that high glycemic index
carbohydrate diet increased diurnal rhythm of
leptin.
7
Consumption of 80% carbohydrate in 13
lean and overweight men had not shown a
significant difference in concentration of leptin.
However, oxidation of carbohydrate was
substantially lower in obese subjects that may be
due to leptin resistance in obese individuals.
17
One parallel intervention study conducted among
18 men and women individuals suggested that
adherence to high carbohydrate diet [65%
carbohydrate (CHO), 15% fat, 20% protein] had not
significant effect on concentration of leptin in
comparison with subjects consumed control diet (45%
CHO, 30% fat, 20% protein). This diet enhanced
leptin sensitivity.
5
It seems that leptin response
implicate after consumption of carbohydrate meals
among obese subjects,
8,17
one cross-sectional study
conducted among 165 overweight and obese women,
in the age range of 50-75 years, showed that significant
inverse association between consumption of habitual
high carbohydrate and fat intakes and leptin
concentration after adjustment for potential
confounders (β = −0.11, P = 0.04).
16
Adherence to
diet rich in fruits, vegetables and fiber with lower
amounts of fat during 12 months had not showed the
substantial effect on leptin level in healthy women.
18
Fats intake and leptin levels: most studies
regarding the relationship between high-fat diet and
concentration of leptin were found that there is a
positive association between intake of higher fats
and leptin level.
8,31
Furthermore, type of fats
including SFA, MUFA and PUFA play the key roles
on augmentation or reduction of circulating leptin
concentration.
1,19,21,25
However, contradictory results
were observed in this regard.
14,26
One cross-sectional study conducted among
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individuals with type 1 diabetes had shown that men
consumed more SFA had more concentration of
leptin.
19
Consumption of linoleic acid and
arachidonic acids among women had a positive and
negative correlation with serum levels of leptin,
respectively.
19
In one parallel clinical trial conducted
among 55 obese subjects, adherence to diet rich in
α-linolenic acid source (rapeseed oil) in 4 weeks led
to increase in serum level of leptin compared with
individuals who followed the diet rich in MUFA
and ɷ
6
sources (olive oil and sunflower oil,
respectively).
1
High-fat diet substantially enhanced plasma level
of leptin in rats.
31
In one parallel intervention study,
consumption of the meal with 70 g fat and 36 g
protein showed no significant change in postprandial
leptin among 19 lean and obese women compared to
high carbohydrate diet.
8
In one experimental study
rats, fed fish oil and safflower oil energy restricted
diet had 62% reduction in leptin levels compared to
beef tallow fed.
21
In contrast, energy-restricted diet
independent of the type of fats could increase leptin
production in rats.
14
Protein intake and leptin levels: fewer studies
examining the effect of high protein diet on leptin
concentration.
13,15
It seems that high protein low-
calorie diet tend to increase in leptin activity.
15
Results from one parallel clinical trial conducted
among 19 participants (men and women) indicated
that adherence to high protein diet (30% protein) in
2 weeks of iso-calorie diet did not enhance the area
under curve (AUC) of leptin compared to control
diet (15% protein). Furthermore, leptin AUC
markedly decreased during 12 weeks energy
restricted high protein diet.
15
It seems that higher
protein intake could increase leptin sensitivity
despite any increase in the hormone
concentration.
15
Augmentation of high dietary
protein during second trimester of gestation led to
significantly increase plasma level of leptin in one
experimental study.
13
Results from other
experimental investigation found no substantial
effect of high protein diet on serum level of leptin.
27
One intervention study conducted among 17
non-diabetic male suggested that low protein diet
(0.6 g/kg) decrease plasma level of leptin that not to
be mediated through insulin-related mechanism.
32
In contrast, serum leptin concentration was
markedly greater in rats with low protein diet, and
food intake enhanced due to augmentation of leptin
in one experimental study.
33
Increase of leptin
concentration suggested that low protein diet might
lead to the state of leptin resistance.
33
Energy intake and concentration of leptin: it
seems that energy restriction reduces concentration
of leptin and high energy intake induces state of
leptin resistance.
7,34,35
A cross-sectional study
conducted among a sample of patients with liver
cirrhosis showed that there is an inverse relationship
between fasting leptin and resting energy
expenditure. Energy intake was found to have no
substantial correlation with fasting concentration of
leptin
7
Serum level of leptin was substantially
negatively correlated with dietary energy intake in
obese individuals in one cross-sectional study
among a sample of Japanese-American in Hawaii
and Japanese in Japan.
34
One intervention study
conducted among 44 healthy men suggested that
energy restricted diet decreased 39.4% fasting leptin
concentration.
35
Discussion
Findings from several studies suggest that a diet
display an important role on change the
concentration of leptin.
5,8,15
It seems that beside the
amount of fats, type of fatty acids have the key roles
on circulating leptin concentration.
1,2
Energy intake
also significantly associated with the hormone.
34,35
Carbohydrate intake has an important role on
regulation of leptin level that may be due to change
in insulin secretion.
8
It is supported by evidence that
carbohydrate meal induces greater postprandial
leptin concentrations than fat meal.
28
According to
evidence leptin deficiency leads to state of obesity,
as well as insulin resistance and glucose tolerance
impairment.
29
In the other hand, obese subjects
have more concentration of leptin that tends to be
the state of leptin resistance.
36
In addition,
concentration of leptin implicates in subjects with
Types 1 and 2 diabestes.
37,38
Obesity is one of the important factors in the
etiology of metabolic syndrome, diabetes and
cardiovascular diseases
39-41
and dietary intakes have
the important role on controlling the obesity and
chronic diseases.
31
Consumption of high glycemic
load of carbohydrates enhance concentration of the
hormone.
6
In addition, intake of the high amount of
fiber causes to increase the leptin sensitivity and
controls the secretion of leptin.
42
It is possible that
the leptin response is different in diverse types of
carbohydrates. Also, the effect of high carbohydrate
intake on leptin concentration may implicate in
obese subjects.
8
Sex and body fat are two most important factors
in concentration of leptin that are supported by
evidence.
43
Weight loss and starvation also can
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decrease circulating of leptin.
44
According to
evidence, SFA enhance the risk of obesity that may
be mediated through a change in concentration of
the hormone. Experimental studies showed that
high-fat diets may elevate the leptin
concentration.
44,45
It seems that a diet rich in MUFA and PUFA
decrease the concentration of the hormone especially
in women compared to SFA.
1
Dietary patterns rich in
MUFA and PUFA usually characterized by high
amount of fiber sources as well as low glycemic index
of carbohydrate that lead to the lower concentration
of leptin.
46
Given the important role of estrogen on
expression of leptin, it is possible that the type of
fatty acids has more effects on women than men.
1
To the best of our knowledge, fewer evidence is
available regarding the impact of high protein diet
on leptin concentration. It seems that higher protein
intake increases satiety and enhances the leptin
concentrations in CNS as well as elevates leptin
sensitivity which tends to be weight maintenance.
15
However, different protein sources were found to
have diverse effects on health status.
47,48
Based on studies, individuals who consumed
more energy from protein were found to have
greater satiety. Increase in dietary protein intakes
promotes an inverse energy balance and body fat
loss. On the other hand, protein intake tends to
increase energy expenditure that may be related to
leptin action.
1
Conclusion
Findings from several studies suggest that a diet
display an important role on change the
concentration of lepton.
Acknowledgments
Isfahan University of Medical Sciences, Iran
supported this paper.
Conflict of Interests
Authors have no conflict of interests.
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... Proses penurunan kadar HDL pada kelompok diet tinggi karbohidrat berlangsung lebih lama dibandingkan dengan kelompok diet tinggi lemak. Hal ini disebabkan oleh diet tinggi lemak dapat menurunkan sensitivitas hormon leptin yang menyebabkan penurunan kadar hormon leptin (Izadi, et al., 2014). ...
... Kadar leptin yang rendah berdampak pada peningkatan nafsu makan pada kelompok diet tinggi lemak sehingga proses penurunan kadar HDL menjadi lebih cepat dibandingkan dengan kelompok diet tinggi karbohidrat. Sebaliknya, peningkatan kadar leptin terjadi pada kelompok diet tinggi karbohidrat sehingga pada kelompok tersebut mengalami penurunan nafsu makan akibat asupan glukosa yang tinggi pada komposisi dietnya (Izadi, et al., 2014). Diet tinggi lemak jenuh dan karbohidrat mampu menginduksi perubahan metabolisme yang mengakibatkan peningkatan kadar partikel small dense LDL (Chiu, et al., 2017). ...
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Atherosclerosis is a condition in which the arteries harden due to the build-up of cholesterol plaques. Atherosclerosis can trigger various degenerative diseases such as coronary heart disease (CHD). Atherosclerosis can occur due to high levels of cholesterol in the blood and triglyceride risk factor associated with excessive carbohydrate consumption. Many cases of cardiovascular disease occur in populations with high carbohydrate consumption. This is attributed to the atherogenic nature of carbohydrates. Excess glucose from carbohydrate metabolism will be synthesized by the liver into triglycerides and stored in adipose tissue and can lead to obesity. High-carbohydrate diet is associated with lower levels of total cholesterol, LDL-C, HDL-C and ApoA. In particular, pure carbohydrates such as sugar contained in ultra-processed food and beverage products are associated with an increased risk of coronary heart disease. Considering the negative effects of high-carbohydrate diet, especially refined carbohydrates, it is necessary to emphasize the importance of choosing carbohydrate sources, reducing added sugars intake such as sucrose and high fructose corn syrup, and also consume whole food, natural, and plant-based, such as vegetables and fruits. Keywords : atherogenic, atherosclerosis, high-carbohydrate diet, plant-based, whole food
... Conversely, decrease in leptin level results to an opposite effect which is inhibition of the satiety center and stimulation of the feeding center and consequently increase in appetite. [24,25] This however could be the reason for the increased food intake observed in the flavonoid administered groups. ...
... This finding could be as a result of decreased leptin concentration in the experimental dams which caused increase in appetite and consequently increase in food intake. This increase in food intake may have caused increase in nutrients secreted from the dams to the pups through the breast milk which lead to the dose dependent increase in the body weight of the pups as observed from this study because leptin has a critical role on regulation of body weight, body fat mass, appetite, and food intakes as it has been earlier stated by Izadi et al. [25] ...
... It is affected, therefore, by the type of diet and the amounts of fat consumed. 90 Interestingly, leptin's action on the hippocampus 91,92 is suggested to be protective against seizures. 93,94 By decreasing serum insulin levels 95 and increasing serum leptin levels, [95][96][97][98] the KD seems to have a favorable metabolic profile underlying its anticonvulsive properties. ...
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The prevalence of obesity tripled worldwide between 1975 and 2016, and it is projected that half of the US population will be overweight by 2030. The obesity pandemic is attributed, in part, to the increasing consumption of the high-fat, high-carbohydrate Western diet, which predisposes to the development of the metabolic syndrome and correlates with decreased cognitive performance. In contrast, the high-fat, low-carbohydrate ketogenic diet has potential therapeutic roles and has been used to manage intractable seizures since the early 1920s. The brain accounts for 25% of total body glucose metabolism and, as a result, is especially susceptible to changes in the types of nutrients consumed. Here, we discuss the principles of brain metabolism with a focus on the distinct effects of the Western and ketogenic diets on the progression of neurological diseases such as epilepsy, Parkinson's disease , Alzheimer's disease, and traumatic brain injury, highlighting the need to further explore the potential therapeutic effects of the ketogenic diet and the importance of standardizing dietary formulations to assure the reproducibility of clinical trials.
... It is affected, therefore, by the type of diet and the amounts of fat consumed. 90 Interestingly, leptin's action on the hippocampus 91,92 is suggested to be protective against seizures. 93,94 By decreasing serum insulin levels 95 and increasing serum leptin levels, [95][96][97][98] the KD seems to have a favorable metabolic profile underlying its anticonvulsive properties. ...
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The prevalence of obesity tripled worldwide between 1975 and 2016, and it is projected that half of the US population will be overweight by 2030. The obesity pandemic is attributed, in part, to the increasing consumption of the high-fat, high-carbohydrate Western diet, which predisposes to the development of the metabolic syndrome and correlates with decreased cognitive performance. In contrast, the high-fat, low-carbohydrate ketogenic diet has potential therapeutic roles and has been used to manage intractable seizures since the early 1920s. The brain accounts for 25% of total body glucose metabolism and, as a result, is especially susceptible to changes in the types of nutrients consumed. Here, we discuss the principles of brain metabolism with a focus on the distinct effects of the Western and ketogenic diets on the progression of neurological diseases such as epilepsy, Parkinson’s disease, Alzheimer’s disease, and traumatic brain injury, highlighting the need to further explore the potential therapeutic effects of the ketogenic diet and the importance of standardizing dietary formulations to assure the reproducibility of clinical trials.
... Ghrelin acts on NPY-producing neurons in the hypothalamus which cause the release of NPY (Kohno et al. 2003). Food intake restores deficits in nutrients, decreasing ghrelin and causes the release of leptin from adipose tissue (Izadi et al. 2014). Leptin acts on NPY-producing neurons in the hypothalamus, reducing the amount of NPY released (Baver et al. 2014). ...
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Rhythmic gene expression is found throughout the central nervous system. This harmonized regulation can be dependent on- and independent of- the master regulator of biological clocks, the suprachiasmatic nucleus (SCN). Substantial oscillatory activity in the brain’s reward system is regulated by dopamine. While light serves as a primary time-giver (zeitgeber) of physiological clocks and synchronizes biological rhythms in 24-h cycles, nonphotic stimuli have a profound influence over circadian biology. Indeed, reward-related activities (e.g., feeding, exercise, sex, substance use, and social interactions), which lead to an elevated level of dopamine, alters rhythms in the SCN and the brain’s reward system. In this chapter, we will discuss the influence of the dopaminergic reward pathways on circadian system and the implication of this interplay on human health.
... Typically, when leptin levels increase, satiety would improve, and weight loss or maintenance occur. However, as leptin is produced in adipose tissue 25 , as fat mass increases, leptin production increases 26,27 . Weight gain is also associated with a decreased sensitivity to leptin 27 , reducing the ability to achieve satiety. ...
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Abstract To examine the effect of a Caralluma Fimbriata extract (CFE) on biomarkers of satiety and body composition in overweight adults. A double-blind, randomised, placebo controlled trial to examine the effect of a Caralluma Fimbriata extract (CFE) on biomarkers of satiety and body composition in overweight adults. Eighty-three men and women aged between 20 and 50 years of age completed 16 weeks of daily supplementation with either CFE or placebo. Plasma cardiometabolic (lipid profile, glucose, insulin) and satiety (ghrelin, leptin, neuropeptideY) biomarkers, body composition, diet history and gastrointenstinal function were assessed at baseline, weeks 4, 8, 12 and 16. Subjects in the CFE and placebo groups were well matched and predominatly female 93% and 87.5%, with a mean age of 40.9 ± 6.7 and 39.5 ± 7.5 years and body mass index (BMI) of 30.0 ± 3.1 and 30.2 ± 2.9 kg/m2 respectively. There was a significant difference in plasma leptin concentration change between groups at week 16 (p = 0.04), with the placebo group increasing concentration (2.27 ± 4.80 ng/mL) while the CFE group (0.05 ± 4.69 ng/mL) remained the same. At week 16, the CFE group had significantly reduced their calorie intake from baseline compared to the placebo group (245 cal vs 15.8 cal respectively p
... The first is limitation of leptin entry through the blood-brain barrier to central nervous system (CNS) [28] and the second is inhibition of leptin receptor expression and second messenger signaling primarily signal transducer and activator of transcription-3 in CNS [29]. The evidences regarding to the effect of dietary components on leptin levels are somewhat controversial [17,[30][31][32]. On the other hand, it has been shown that leptin has a circadian rhythm and therefore interacts with genes that regulate circadian rhythms [33]. ...
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Circadian disruption causes obesity and other metabolic disorders. There is no research considering the role of Cryptochromes (Cry) 1 body clock gene and major dietary patterns on serum leptin level and obesity. We aimed to investigate the interaction between Cry1 circadian gene polymorphisms and major dietary patterns on leptin and obesity related measurements. This study was performed on 377 overweight and obese women. Mean age and body mass index (BMI) of study subjects were 36.64 ± 9.02 years and 30.81 ± 3.8 kg/m2, respectively. Dietary assessment was done using a validated 147-item food frequency questionnaire. Cry1 rs2287161 were genotyped using polymerase chain reaction-restriction fragment length polymorphism. Generalized linear models were used for interaction analysis. Healthy and unhealthy dietary pattern (HDP and UDP, respectively) were extracted using factor analysis (principal component analysis). Our study revealed a significant higher weight (p = 0.003) and BMI (p = 0.042) in women carrying CC homozygote compared with G allele carriers. Moreover, our findings showed a significant gene-diet interaction between HDP and Cry1 rs2287161 on BMI (p = 0.034) and serum leptin level (p = 0.056) in which, BMI and serum leptin level were lower in subjects with CC genotype than in those with GG genotype while following HDP. This study suggests a significant interaction between Cry1 rs2287161 polymorphisms and HDP on BMI and serum leptin and the lowering effects were apparent among C allele carriers compared to G allele ones. This data highlights the role of dietary pattern in relation of gene and obesity.
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Controlling mechanisms of appetite and food intake is an important issue for a variety of different types of athletes. Previous studies showed omega-3 fatty acid increased appetite in patients, but results in healthy individuals are inconclusive. This study assessed the effect of omega-3 fatty acid supplements on food intake and appetite in young male athletes with normal body fat percentage. In a three-week double-blind placebo-controlled RCT in Tabriz, Iran (2019), 72 male athletes, age 22.2 (±2.5) y with 13.9 (8.5) body fat percent were randomized to either an omega-3 (2000 mg/day; EPA: 360 mg, DHA: 240 mg) or placebo (2000 mg/day paraffin) group. 3-day food diaries were completed before and after the intervention. Body composition was measured by bioelectrical impedance analysis. Appetite was assessed by visual analog scale (VAS) before and after each week of intervention. Results showed carbohydrate intake increased in the omega-3 group (MD = 65.8 g; 95% CI = 9.1, 70.1; P = 0.03). VAS score for satiety decreased. Hunger sensation, desire to eat, and desire to eat sweet foods increased in each of the three weeks. In conclusion, our findings showed that omega-3 supplementation increased appetite in healthy athletes without significant change in body fat percentage. Further research is needed to generalize the results to other populations.
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For physical therapists, one of the primary aims is to improve public health by promoting and re-establishing healthy sleep patterns. In-depth knowledge of sleep physiology is essential for developing and validating more accurate diagnostic tools, developing innovative patient management systems, and being up to date with the latest advancements in sleep medicine. Sleep is an essential physiological process for the proper maintenance of a body’s homeostasis and health, supporting a wide range of systems. In addition, the relationship between systems and physiological regulation of sleep presents different characteristics depending on the sleep stage.
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Background: Diabetes mellitus, increased blood glucose or hyperglycemia, is associated with increased oxidative stress and cardiovascular diseases. This condition will further cause carbohydrate and fat metabolism change, resulting in the decreased antioxidant defense system. Black rice, red beans, and moringa leaves contain oleic acid, butyric amino acid, antioxidants, phytic acid, and arginine, which can improve insulin sensitivity, and blood glucose homeostasis. Objective: This study aimed to analyze the effect of betamelor (black rice, red beans, and moringa leaves) on blood glucose in rats Materials and Methods: The design of this research was experimental research with pre-and post-control group design. A total of 20 Sprague Dawley female rats were divided into four groups, namely standard feed (PS), 80% feed of betamelor (PB8), 50% feed of betamelor (PB5), and 20% feed of betamelor (PB2). Betamelor intervention was given as much as 5% of weight for 28 days. Fasting Blood Glucose (FBG) levels were measured using the GOD-PAP method. Blood glucose data were analyzed by Analysis of Variance (ANOVA) at a 95% confidence level and using Duncan's test. Results: There were differences in FBG between groups after the intervention of betamelor. The results showed that after 28 days of intervention, betamelor decreased the serum glucose concentration from 122.69 mg / dL to 97.70 mg / dL (20.37%) in the PB8 group and from 123.91 mg / dL to 113.28 mg / dL (8.58%) in the PB5 group, but the standard diet (PS) increased by 5.73%. This result can be applied to reduce blood glucose levels in obese and patients with metabolic syndrome. Conclusions: There was a significant effect of giving a mixture of black rice, red beans, and Moringa leaves on fasting blood sugar in rats.
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Studies regarding the effects of high protein (HP) diets on cardiovascular (CVD) risk factors have reported contradictory results. We aimed to determine the effects of an HP diet on CVD risk factors and high-sensitivity C-reactive protein (hs-CRP) among overweight and obese women. In this randomized controlled trial, we recruited 60 overweight and obese women, aged 20-65, into an HP or energy-restricted control diet for three months (protein, carbohydrate, and fat: 25%, 45%, and 30% versus 15%, 55%, and 30%, resp.). Total protein was divided between animal and plant sources in a 1 : 1 ratio, and animal sources were distributed equally between meats and dairy products. Fasting blood samples, hs-CRP, lipid profile, systolic and diastolic blood pressure, and anthropometric measurements were assessed using standard guidelines. Percent change was significantly different between the two diet groups for weight (standard protein (SP): -3.90 ± 0.26 versus HP: -6.10 ± 0.34%; P < 0.0001, resp.) and waist circumference (SP: -3.03 ± 0.21 versus HP: -5.06 ± 0.28%; P < 0.0001, resp.). Percent change of fasting blood glucose (FBG) substantially decreased in the control group compared to the HP group (-9.13 ± 0.67 versus -4.93 ± 1.4%; P = 0.01, resp.). Total cholesterol, systolic blood pressure (SBP), and diastolic blood pressure (DBP) decreased both in the HP and in the control diet groups (P = 0.06, P = 0.07, and P = 0.09, resp.); however, the results were marginally significant. Serum levels of hs-CRP were reduced both in the control (-0.08 ± 0.11%, P = 0.06) and in the high protein groups (-0.04 ± 0.09%, P = 0.06). The energy-restricted HP diet resulted in more beneficial effects on weight loss and reduction of waist circumference. CVD risk factors may improve with HP diets among overweight and obese women. When using isoenergetic weight loss diets, total cholesterol, hs-CRP, and SBP were marginally significantly reduced, independent of dietary protein content. This trial is registered with ClinicalTrials.gov NCT01763528.
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Leptin is produced by mature adipocytes. Its amount correlates positively with the mass of the adipose tissue. Leptin plays a crucial role in maintaining body weight and glucose homeostasis. It is transported through the blood-brain barrier to the central nervous system, where it activates the autonomic nervous system, causing the feeling of satiety and inhibiting appetite. It also acts through central and peripheral pathways, including the regulation of insulin secretion by pancreatic  cells. Leptin may also directly affect the metabolism and function of peripheral tissues. It has been found to play a role in peripheral insulin resistance by attenuating insulin action, and perhaps also insulin signaling, in various insulin-responsive cell types. Recent data provide convincing evidence that leptin has a beneficial influence on glucose homeostasis. Studies suggest that leptin could be used as an adjunct of insulin therapy in insulin-deficient diabetes, thereby providing an insight into the therapeutic implications of leptin as an anti-diabetic agent. Extensive research will be needed to determine long-term safety and efficacy of such a therapy.
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Ghrelin is a polypeptide that is excreted by the secretory cells of the gastric and intestinal mucosa, the arcuate nucleus of the hypothalamus as well as by the epsilon cells (ε) located in the pancreatic islets. It plays an important role in maintaining the energy balance of the organism and influences the endocrine function of the pancreas and glucose metabolism. It takes part in the regulation of glucose homeostasis through the modulation of insulin secretion and insulin sensitivity. Due to the broad spectrum of ghrelin's biological effects, ways to modify them are presently being investigated. Much attention is focused on the enzyme called ghrelin O-acyl transferase (GOAT), which mediates the physiological functions of ghrelin. Acyl-ghrelin and des-acyl-ghrelin appear to have opposite glucoregulatory effects. The regulation of acylation by GOAT seems therefore to play a role in mediating glucose metabolism. The modulation of GOAT or ghrelin signaling may be a clinically relevant strategy to treat obesity and metabolic diseases such as type 2 diabetes.
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Intake of whole grains is inversely associated with risk of diabetes and ischemic heart disease in observational studies. The lower risk associated with high whole-grain intakes may be mediated through improvements in glycemic control, lipid profiles, or reduced inflammation. The aim was to examine whether the intake of whole grains, bran, and germ is related to homocysteine, plasma markers of glycemic control (fasting insulin, hemoglobin A1c, C-peptide, and leptin), lipids (total cholesterol, triacylglycerol, HDL cholesterol, and LDL cholesterol), and inflammation (C-reactive protein, fibrinogen, and interleukin 6). This was a cross-sectional study of the relations of whole grains, bran, and germ intakes with homocysteine and markers of glycemic control, lipids, and inflammation in 938 healthy men and women. Whole-grain intake was inversely associated with homocysteine and markers of glycemic control. Compared with participants in the bottom quintile of whole-grain intake, participants in the highest quintile had 17%, 14%, 14%, and 11% lower concentrations of homocysteine (P < 0.01), insulin (P = 0.12), C-peptide (P = 0.03), and leptin (P = 0.03), respectively. Inverse associations were also observed with total cholesterol (P = 0.02), HDL cholesterol (P = 0.05), and LDL cholesterol (P = 0.10). Whole-grain intake was not associated with the markers of inflammation. Whole-grain intake was most strongly inversely associated with markers of glycemic control in this population. The results suggest a lower risk of diabetes and heart disease in persons who consume diets high in whole grains.
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Background: Although previous studies showed some benefits from dairy consumption with respect to obesity and insulin resistance syndrome, epidemiologic data on the association between dairy intakes and metabolic syndrome are sparse. Objective: The objective was to evaluate the relation between dairy consumption and metabolic syndrome in Tehranian adults. Design: Dairy consumption and features of metabolic syndrome were assessed in a population-based cross-sectional study of 827 subjects (357 men and 470 women) aged 18–74 y. Metabolic syndrome was defined according to guidelines of the Adult Treatment Panel III. Multivariate logistic regression adjusted for lifestyle and nutritional confounders was used in 4 models. Results: Mean (±SD) consumption of milk, yogurt, and cheese was 0.7 ± 0.2, 1.06 ± 0.6, and 0.9 ± 0.3 servings/d, respectively. Subjects in the highest quartile of dairy consumption had lower odds of having enlarged waist circumference [odds ratio (OR) by quartile: 1, 0.89, 0.74, 0.63; P for trend < 0.001], hypertension (OR by quartile: 1, 0.88, 0.79, 0.71; P for trend < 0.02), and metabolic syndrome (OR by quartile: 1, 0.83, 0.74, 0.69; P for trend < 0.02). The values of ORs became weaker after further adjustment for calcium intake. Conclusion: Dairy consumption is inversely associated with the risk of having metabolic syndrome. It seems that this relation is somewhat attributed to calcium.
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Background: Ad libitum, low-carbohydrate diets decrease caloric intake and cause weight loss. It is unclear whether these effects are due to the reduced carbohydrate content of such diets or to their associated increase in protein intake. Objective: We tested the hypothesis that increasing the protein content while maintaining the carbohydrate content of the diet lowers body weight by decreasing appetite and spontaneous caloric intake. Design: Appetite, caloric intake, body weight, and fat mass were measured in 19 subjects placed sequentially on the following diets: a weight-maintaining diet (15% protein, 35% fat, and 50% carbohydrate) for 2 wk, an isocaloric diet (30% protein, 20% fat, and 50% carbohydrate) for 2 wk, and an ad libitum diet (30% protein, 20% fat, and 50% carbohydrate) for 12 wk. Blood was sampled frequently at the end of each diet phase to measure the area under the plasma concentration versus time curve (AUC) for insulin, leptin, and ghrelin. Results: Satiety was markedly increased with the isocaloric high-protein diet despite an unchanged leptin AUC. Mean (±SE) spontaneous energy intake decreased by 441 ± 63 kcal/d, body weight decreased by 4.9 ± 0.5 kg, and fat mass decreased by 3.7 ± 0.4 kg with the ad libitum, high-protein diet, despite a significantly decreased leptin AUC and increased ghrelin AUC. Conclusions: An increase in dietary protein from 15% to 30% of energy at a constant carbohydrate intake produces a sustained decrease in ad libitum caloric intake that may be mediated by increased central nervous system leptin sensitivity and results in significant weight loss. This anorexic effect of protein may contribute to the weight loss produced by low-carbohydrate diets.
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Purpose: It has been hypothesized that leptin-induced appetite suppression is impaired in obese individuals, but little human evidence is available documenting this. We investigated relations between serum leptin and total energy intake using INTERLIPID/INTERMAP data on Japanese-Americans in Hawaii and Japanese in Japan. Methods: Serum leptin and nutrient intakes were examined by standardized methods in men and women aged 40-59 years from two population samples, one Japanese-American in Hawaii (88 men, 94 women), the other Japanese in central Japan (123 men, 111 women). Multiple linear regression analyses stratified by BMI category (<25 kg/m(2), 25-29.9 kg/m(2), and ≥ 30 kg/m(2)) with adjustment for possible confounders were used to examine the relation between log-leptin and total dietary energy intake. Results: In multivariate regression analyses, in those with BMI < 25 kg/m(2) and in those with BMI between 25 and 29.9 kg/m(2), log-leptin was not significantly related to total dietary energy intake; in those with BMI ≥ 30 kg/m(2), it was significantly inversely related to total dietary energy intake (P = 0.029), independent of body weight and physical activity. Physical activity score was significantly positively related to total dietary energy intake only in participants with BMI < 25 kg/m(2) (P < 0.001). Conclusion: Leptin was significantly inversely associated with dietary energy intake in obese persons, but not in overweight and normal-weight persons.
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The objective of this study was to evaluate the effects of in utero and postnatal exposure of a high-protein (HP; n=9) or moderate-protein (MP; n=16) diet on growth, and serum metabolite, ghrelin and leptin concentrations during the first 4 months of life in kittens. It was hypothesized that blood indices would be modified due to diet. Blood samples were collected from kittens at 4, 8, 12 and 16 weeks of age. Kittens were weaned at 8 weeks of age onto the same diet as the dam. Body weight was measured weekly from birth and daily food intake for each litter was recorded post-weaning. Serum concentrations of urea nitrogen, total protein and triglycerides were greater (P<0.05) in kittens fed the HP diet. Serum cholesterol concentrations were greater (P <0.05) in MP-fed kittens at 4 weeks of age. Moderate-protein fed kittens tended to have greater (P < 0.10) serum ghrelin concentrations. Leptin concentrations were not affected by diet, but changed over time (P<0.05). Our data indicate that diet and age of kittens affect circulating concentrations of peptides important in appetite regulation. Further research testing the effects of in utero and early postnatal nutrient exposure on feline obesity risk in adulthood is needed.