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Lipid metabolic alterations and satiety with a pumpkin-based supplement in obese dogs
Abstract
Objective-To evaluate the combined effects of a dietary fiber and carnitine supplement using a commercially available canned dog supplement on satiety, weight loss, and lipid metabolism. Design-A randomized, crossover design (satiety study) and randomized complete block design (weight loss study) Sample Population-12 (satiety study) and 7 (weight loss study) adult female overweight/ obese Beagles. Procedures-Two studies were conducted. In the satiety study, dogs were fed 1.2 times maintenance energy amounts of either high dietary fiber/high carnitine (HF/C) or low dietary fiber/low carnitine (LF/C) supplemented diet twice a day using a 3 hour interval and food intake was monitored. Blood samples were obtained at 0, 45, and 120 min postprandially for peptide YY determination. For the weight loss study, 60 % of maintenance energy amounts of either the HF/C or LF/C diet were fed for 42 days. Blood samples were collected at days 1, 28, and 42 to determine plasma lipid metabolites and peptide YY. Results-The HF/C diet decreased both the amount of food and energy intakes at 3 hour post-feeding, suggesting improved 3 hour post-meal satiety. This combination supplement also increased postprandial plasma β-hydroxybutyrate at day 42 and was associated with greater body fat and weight loss without alteration of plasma peptide YY, triglyceride, total cholesterol, and lipoprotein- cholesterol concentrations. Conclusions and Clinical Relevance- The combination of dietary fiber/carnitine from a commercially available canned supplement demonstrated the potential to decrease begging behavior between meals due to increased 3 hour post-meal satiety. This combination supplement also supported improved body weight reduction and increased fat utilization without altering plasma triglyceride, lipoprotein-cholesterol and cholesterol concentrations.
... LG and LG, no difference was observed in the present study, as well as in the study published by Ferreira et al. [22]. In another study with dogs, similarly to our results, the administration of a diet composed of high soluble fiber levels was not sufficient to increase the serum PYY concentrations in obese animals [44,45]. ...
... Both PYY and GLP-1 increase the gastric emptying time and small intestine transit time [45]. These effects may lead to prolonged gastric distension and, consequently, signs of satiety [44,45], as well as delayed nutrient contact with the small intestinal receptors involved in maintaining satiety. Prolonged gastric emptying can also impair starch digestion and consequently glucose absorption, hence improving post-prandial glucose and insulin concentration stability [46,48]. ...
Background
Obesity is one of the most common nutritional disorders in dogs and cats and is related to the development metabolic comorbidities. Weight loss is the recommended treatment, but success is difficult due to the poor satiety control. Yeast beta-glucans are known as biological modifiers because of their innumerable functions reported in studies with mice and humans, but only one study with dogs was found. This study aimed to evaluate the effects of a diet supplemented with 0.1% beta-glucan on glucose, lipid homeostasis, inflammatory cytokines and satiety parameters in obese dogs. Fourteen dogs composed three experimental groups: Obese group (OG) with seven dogs with body condition score (BCS) 8 or 9; Lean group (LG) included seven non-obese dogs with a BCS of 5; and Supplemented Obese group (SOG) was the OG dogs after 90 days of consumption of the experimental diet.
Results
Compared to OG, SOG had lower plasma basal glycemic values (p = 0.05) and reduced serum cholesterol and triglyceride levels. TNF-α was lower in SOG than in OG (p = 0.05), and GLP-1 was increased in SOG compared to OG and LG (p = 0.02).
Conclusion
These results are novel and important for recognizing the possibility of using beta-glucan in obesity prevention and treatment.
... However, it is difficult to compare our data with the literature due to some limitations in the experimental design (feed administration and sampling). The obtained results suggest that specific characteristics of these ingredients and their level of inclusion affected glycemic response (19,20). The GF1 diet always reported the lowest values of glucose and insulin AUC. ...
Introduction
Dog owners have gradually changed their approach, paying more attention to the nutrition and health of their animals. Various pet foods with different ingredients and nutritional characteristics are available on the market. The present study aimed to evaluate the administration of three diets, namely, two grain-free (GF1 and GF2) and one grain-based (CB), with different sources of carbohydrates that can influence the glycemic and insulin postprandial responses in healthy dogs.
Materials
Fifteen healthy dogs were dived in three groups and alternatively fed each diet for 50 days. Blood samples were collected at beginning of each feeding period. Glycemia and insulin were measured before and after 120, 240 and 360 minutes diet administration to evaluate postprandial responses.
Results
GF2 diet showed the highest level of albumin and mean insulin concentration (p < 0.001). Furthermore, the GF1 diet caused the smallest (p < 0.001) glucose and insulin area under the curve (AUC) and the lowest (p < 0.05) glucose nadir. Otherwise, GF1 showed the highest (p < 0.01) insulin time to peak. The GF2 diet showed the highest level of albumin while reporting the lowest amount of fructosamine (p < 0.05). The diet GF2 registered the highest (p < 0.001) level of insulin zenith. The cereal-based (CB) diet reported the highest amount of fructosamine (p < 0.05). The CB diet had the highest levels of glucose and the highest (p < 0.001) glucose and insulin mean concentrations. Diet CB reported the lowest (p < 0.001) insulin nadir.
Discussion
Diets with different carbohydrate sources and chemical compositions could modulate the glycemic response in healthy dogs. Bearing in mind that glycemic/insulin postprandial responses influence energy availability and that different dogs have specific lifestyles, it may be preferable to also consider these aspects when choosing a maintenance diet for animals
Superfruit-positioned dog foods Superfruits, a subcategory of superfoods, are portrayed as fruits with outstanding health-promoting properties that are linked to their composition. The term superfruit is not regulated and can be applied as a marketing tool to any fruit. Superfruits in the human food market have made their way to preprocessed components of kibbled and canned petfood. Petfood superfruit ingredients include pomegranate, avocado, pumpkin, cranberry and blueberry. The addition may be highlighted on the packaging or websites. The words pumpkin, cranberry and blueberry form part of the product name of certain petfoods. The name of a petfood brand features part of the word pomegranate and another one displays a shortening of avocado. Superfruit is lauded for being packed with vitamins. As a constituent of complete and balanced petfood this is not relevant. These formulas by definition meet the all nutrient needs of dogs with ample safety margins. For superfruit in petfood, the prefix " super " is appropriate only if the inclusion has a proven health-promoting effect in dogs. This requires that the fruit possesses biological activity, which survives the processing steps and is present in the food at an effective level. Petfoods may not make explicit health claims on their superfruit accessory, but ride the wave of the aliment's popularity. Dog food containing avocado flesh meal and oil, which lack a known, specific active principle, is purported to enhance skin and hair coat health. Powdered pomegranate seeds, dry pureed pumpkin and dried cranberries and blueberries in dog food are recommended as source of antioxidants. Claimed health benefits comprise supporting immune action, urinary tract, memory function and cardiovascular system. These assertions cannot be substantiated by research data in dogs.
The study reported here investigated the effect of satiety on body composition. Twelve beagle dogs were fed either a low-fiber (< 2%) or a high-fiber (approximately 20%) food that had previously been shown to cause differences in satiety. After 3 weeks the groups were fed the opposite food. Dogs were fed all they would voluntarily consume during one 45-minute meal per day. Each dog served as its own control. Although dogs consumed approximately equal amounts of food on a weight basis, they voluntarily ate significantly fewer calories (27% less) when fed the high-fiber food. Dogs lost four times as much fat mass when fed the high-fiber food versus when fed the low-fiber food. Therefore this study indicates that foods enhanced with fiber increase satiety and reduce adiposity.
The effect of one week of supplementation with a water-soluble fibre (guar gum) was studied in obese women who had lost weight. In study 1 (N=17; mean+/-SEM: age 38.5+/-2.3 yrs; weight 86.8+/-2.3 kg; BMI 32.2+/-0.9 kg.m-2) energy intake and hunger and satiety scores were assessed under free-living conditions. In study 2 (N=14; age 44. 5+/-1.8 yrs; weight 78.8+/-3.1 kg; BMI 29.0+/-0.9 kg.m-2) energy intake was fixed at 6 MJ.day-1 (their normal energy intake at that time) or 4 MJ.day-1 (low energy intake). In both studies, the effect of one week of fibre supplementation (40 g in study 1 and 20 g in study 2) was compared with no supplementation. In study 1, mean energy intake decreased significantly from 6.7+/-0.4 MJ to 5.4+/-0.2 MJ daily after fibre supplementation, while hunger and satiety scores did not change. At a low energy intake level of 4 MJ given in study 2, hunger scores were significantly decreased after fibre supplementation. No changes were seen in hunger and satiety scores during fibre supplementation at 6 MJ. The reduction in energy intake by soluble fibre under free living conditions and the hunger-reducing effect of fibre at the low energy intake level (4 MJ) suggests that fibre may be useful in the treatment of obesity, by facilitating compliance to low energy intake.
Fatty acid oxidation seems to provide an important stimulus for metabolic control of food intake, because various inhibitors of fatty acid oxidation (mercaptoacetate, methyl palmoxirate, R-3-amino-4-trimethylaminobutyric acid) stimulated feeding in rats and/or mice, in particular when fed a fat-enriched diet, and long-term intravascular infusion of lipids reduced voluntary food intake in various species, including humans. The feeding response to decreased fatty acid oxidation was due to a shortening of the intermeal interval with meal size remaining unaffected. Thus, energy derived from fatty acid oxidation seems to contribute to control of the duration of postmeal satiety and meal onset. Since inhibition of glucose metabolism by 2-deoxy-D-glucose affects feeding pattern similarly, and spontaneous meals were shown to be preceded by a transient decline in blood glucose in rats and humans, a decrease in energy availability from glucose and fatty acid oxidation seems to be instrumental in eliciting eating. Since the feeding response of rats to inhibition of fatty acid oxidation was abolished by total abdominal vagotomy and pretreatment with capsaicin destroying non-myelinated afferents and attenuated by hepatic branch vagotomy, fatty acid oxidation in abdominal tissues, especially in the liver, apparently is signalled to the brain by vagal afferents to affect eating. Brain lesions and Fos immunohistochemistry were employed to identify pathways within the brain mediating eating in response to decreased fatty acid oxidation. According to these studies, the nucleus tractus solitarii (NTS) of the medulla oblongata represents the gate for central processing of vagally mediated afferent information related to fatty acid oxidation. The lateral parabrachial nucleus of the pons seems to be a major relay for pertinent ascending input from the NTS. In particular the central nucleus of the amygdala, a projection area of the parabrachial nucleus, appears to be crucial for eating in response to decreased fatty acid oxidation. As ketones are products of hepatic fatty acid oxidation that are released into the circulation and peripheral (and central) administration of 3-hydroxybutyrate reduced voluntary food intake in rats, ketones being utilized as fuels by the peripheral and central nervous system might contribute to control of eating by fatty acid oxidation, especially when high levels of circulating ketones occur. Whether a modulation of the hepatic membrane potential resulting from changes in the rate of fatty acid oxidation and/or ketogenesis represent a signal for control of eating transmitted to the brain by vagal afferents remains to be established. Recent in vivo studies investigating the effects of mercaptoacetate on the hepatic membrane potential and on afferent activity of the hepatic vagus branch are consistent with this notion. Further investigations are necessary to delineate the coding mechanisms by which fatty acid oxidation and/or ketogenesis modulate vagal afferent activity.
Weight gain and risk of type 2 diabetes are inversely associated with a high intake of insoluble cereal fibres. Because nutrient-induced changes of 'satiety hormones' from the gut may play a role in this process, we evaluated the effects of purified insoluble fibres on postprandial responses of plasma peptide YY (PYY), serum ghrelin and satiety as secondary outcome measures of a study investigating effects of cereal fibres on parameters of glucose metabolism. Fourteen healthy women were studied on six occasions in a randomized, single-blind, controlled crossover design. After 24 h run-in periods and 10 h overnight fasts, subjects ingested isoenergetic and macronutrient matched portions of control white bread or fibre-enriched bread (wheat-fibre or oat-fibre) at 08.15 hours. Gut hormones and hunger scores were measured for 300 min. Basal PYY and ghrelin concentrations were not different between the test meals (P>0.15). Postprandial responses of PYY and ghrelin were blunted after the intake of wheat-fibre (total area under the curve (AUC) PYY, 177.9 (SEM 8.1) (pmol/l) min; P=0.016; ghrelin 51.0 (SEM 2.5) (pmol/l) min; P=0.003), but not after oat-fibre (PYY 226.7 (SEM 25.7) (pmol/l) min; P>0.15; ghrelin 46.2 (SEM 1.6) (pmol/l) min; P=0.127), compared to control (PYY 247.5 (SEM 25.6) (pmol/l) min; ghrelin 42.5 (SEM 1.3) (pmol/l) min). Postprandial hunger scores were unaffected by the different test meals (P>0.15). Thus, oat- and wheat-fibre consumption result in different postprandial responses of PYY and ghrelin, but interestingly do not differ in satiety effects.
The aim of the study was to compare the effect of the administration of a mixture of fibres on body weight-loss, satiety, lipid profile and glucose metabolism. We included 200 overweight or obese patients in a parallel, double-blind, placebo-controlled clinical trial, who were randomised to receive, in the context of an energy-restricted diet for a period of 16 weeks, a mixed fibre dose (3 g Plantago ovata husk and 1 g glucomannan) twice (b.i.d. group) or three times daily (t.i.d. group) or placebo. Weight change was the primary efficacy endpoint. Satiety, dietary compliance, lipid profile, glucose tolerance, insulin resistance and high-sensitivity C-reactive protein were secondary endpoints. Weight loss tended to be higher after both doses of fibre (-4.52 (SD 0.56) and -4.60 (SD 0.55) kg) than placebo (-0.79 (SD 0.58) kg); the differences in changes between groups were not statistically significant. Postprandial satiety increased in both fibre groups compared to the placebo. The differences between groups in LDL-cholesterol levels were significant (P = 0.03), with greater reductions in the two fibre-supplemented groups (-0.38 (SD 0.10) and -0.24 (SD 0.09) mmol/l in the b.i.d. and t.i.d. groups v. -0.06 (SD 0.09) mmol/l in placebo group). A similar pattern was observed for changes in total cholesterol:HDL-cholesterol and HDL-cholesterol:LDL-cholesterol ratios. Interventions were well tolerated and had no effects on HDL-cholesterol, glucose and insulin concentrations, glucose tolerance or high-sensitivity C-reactive protein. In conclusion, a 16-week dietary supplement of soluble fibre in overweight or obese patients was well tolerated, induced satiety and had beneficial effects on some CVD risk factors, the most important of which was a significant decrease in plasma LDL-cholesterol concentrations.
Weight-loss programs for dogs are often hampered by increased begging and scavenging behavior that ensues when food intake is restricted.
A diet formulated to contain a high content of both protein and fiber is more satiating than diets that contain only high fiber or high protein.
Six entire female adult dogs (2 Shetland Sheepdogs, 2 Brittany Spaniels, 2 Labrador Retrievers) participated in the satiety studies; 105 adult female dogs of various breeds and ages were used for the palatability studies.
Three diets (high protein [103 g/1,000 kcal] high fiber [60 g/1,000 kcal] [HPHF]; high protein [104 g/1,000 kcal] moderate fiber [35 g/1,000 kcal] [HP]; moderate protein [86 g/1,000 kcal] high fiber [87 g/1,000 kcal] [HF]) were tested. Voluntary food intake was measured in 5 sequential crossover studies, and palatability was assessed with food preference tests.
Protein digestibility was significantly lower for HF (mean +/- SD; 77.7% +/- 2.52%) than for both HPHF (81.1% +/- 0.96%) and HP (81.1% +/- 1.65%) (P < .001). Short-term food intake (food ingested when offered for 15 minutes every hour for 4 hours) was lower for HPHF than for both HP and HF (P = .038). Medium-term intake (food ingested when offered 3 hours after first meal) was lower for both HPHF (27 +/- 22.2 kcal/kg(0.73)) and HF (41 +/- 6.8 kcal/kg(0.73)) than for HP (57 +/- 18.8 kcal/kg(0.73)) (P = .041). Voluntary food intake 3 hours after feeding a restricted meal (25% daily maintenance energy requirements) was significantly lower on the HPHF diet than on either the HP (-51%, P = .0051) or HF (-47%, P = .014) diets. However, there was no significant difference between the energy intake on the HP and HF diets (7%, P = .37). The HPHF and HP diets had equivalent palatability, and both were more palatable than the HF diet (P < .001).
The HPHF diet had a satiating effect as evidenced by reduced voluntary intake compared with HP and HF diets, and has the potential to lead to greater compliance in weight-loss programs.
Inclusion of fiber in the diet has been linked to the prevention of a range of illnesses and conditions. This review contains several ideas about the possible benefits of dietary fiber intake in patients with metabolic syndrome. The principal beneficial effects of a fiber-rich diet in these patients are: prevention of obesity, improved glucose levels, and control of the profile of blood lipids. We now also know that dietary fiber may favor the control of arterial blood pressure. Animal experiments have also shown the benefit of different types of fiber on these variables. Of particular relevance are the studies using obese Zucker rats, which present similar anomalies to those seen in patients with metabolic syndrome. There is therefore a growing interest in discovering new sources of natural fiber. Some of these different kinds of fiber may then be used as functional ingredients to obtain foods with properties that are beneficial to health.
Cholesterol-fed rats which received diets supplemented with 10% pectin, guar gum, or oat bran fiber showed a reduced accumulation of cholesterol and triglyceride in both plasma and the liver. In contrast, an increase in the plasma high-density lipoprotein cholesterol levels of these same rats was noted. This study indicates that certain plant fibers selectively lower plasma total cholesterol while raising high-density lipoprotein cholesterol levels.
It has been suggested that sufficient fiber in the diet will tend to prevent excessive food intake and depot fat accumulation by decreasing the caloric density of the diet, stowing rate of food ingestion, increasing the effort involved in eating, promoting intestinal satiety, and interfering slightly with efficiency of energy absorption. The increase in the prevalence of obesity in Western countries since 1900 has taken place concurrently with marked changes in the nature of the diet. Per capita intake of dietary fiber associated with starchy foods has greatly decreased, but intake of fiber associated with fruits and green vegetables has increased. Thus, although the type of fiber in the diet has changed, the total quantity may not have diminished considerably. Studies of the effect of caloric dilution with cellulose and other metabolically inert bulking agents have disclosed little or no inhibitory effect on the spontaneous energy intake of nonobese laboratory animals and human subjects. Nevertheless, there is evidence that obese rats and humans may defend their excess weight against nutritive dilution with less tenacity than their nonobese counterparts. The hypothesis that dietary fiber can protect against obesity therefore deserves further testing since an increase in the fiber content of the diet may tend to prevent overeating and excessive weight gain even if it does not reduce spontaneous energy intake in nonobese organisms.
We investigated the effects of fiber-rich wheat bran and wheat germ on dietary fat and cholesterol assimilation. Rats were given a test meal containing [14C]triolein and [3H]cholesterol. After various digestion periods, addition of the wheat fractions (10% of meal solids) did not modify the lipid gastric emptying rate. Gastric and intestinal triglyceride lipolysis was significantly reduced when wheat fractions were present. The mucosal uptakes of [14C]lipids and [3H]cholesterol were significantly modified by the wheat fractions after 1 and 2.5 h. No shift in the site of intestinal absorption and no change in the distribution of labeled lipid in the intestinal mucosa was observed. Plasma [14C]lipids and [3H]cholesterol were significantly decreased by both wheat fractions whereas these increased cecal accumulation of dietary lipids and cholesterol. Thus wheat bran and wheat germ alter fat and cholesterol processing in rats. A mechanism of action accounting for the data observed in proposed.
Management of obesity should initially involve assessment of the pet to rule out other possible medical problems and provide an accurate dietary history. It is essential to obtain a good estimate of the existing caloric intake, including calories from table scraps, pet treats, or other sources. Assessing the owner's willingness to make a commitment to a major lifestyle change for their pet is also an important part of any successful weight-reduction program. In some instances, this motivation can be linked to a recent, expensive bill for orthopedic or other procedures performed on their pet. Once a candidate has entered a program, calculated restriction of energy while maintaining protein, vitamin, and mineral intake should be recommended. It may be surprising to find out that the calculated amounts of food may be more than the amount a pet is currently being fed. In these animals, it is imperative to use a high-protein, obesity-management diet and not a low-protein, "light," or senior type of diet containing high fiber. If possible, treats should be restricted altogether and begging actively discouraged. Any snacks should be placed in the pet's feeding bowl so that an association between eating and the bowel become established. Of equal importance is use of a realistic exercise program that owners will encourage their pet to follow. Various products for weight reduction are available. Use of these specially formulated products to restrict caloric intake, while maintaining essential nutrient intake and increasing energy expenditure by playing and other activities, are the hallmarks of successful weight loss programs.
Endocrine L-cells of the distal intestine synthesize both peptide YY (PYY) and proglucagon-derived peptides (PGDPs), whose release has been reported to be either parallel or selective. Here we compare the release mechanisms of PYY, glucagon-like peptide-1 (GLP-1), and oxyntomodulin-like immunoreactivity (OLI) in vivo. Anaesthetized rats were intraduodenally (ID) given either a mixed semi-liquid meal or oleic acid, or they received oleic acid or short chain fatty acids (SCFA) intracolonically (IC). The ID meal released the three peptides with a similar time-course (peak at 30 min); ID oleic acid produced a progressive release of PYY and OLI, while GLP-1 release was less. IC oleic acid or SCFA released smaller (but significant) amounts of PYY but no OLI or GLP-1. Hexamethonium inhibited most of the response to the ID meal and ID oleic acid, but did not change the PYY response to IC oleic acid. N
G
-nitro-l-arginine methyl ester (l-NAME, a nitric oxide synthase inhibitor) inhibited meal-induced PYY release and left OLI and GLP-1 unaffected. BW10 (a gastrin-releasing peptide antagonist) had no effect on the meal-induced release of either peptide. These results suggest a parallel initial release of PYY, OLI and GLP-1 after the ID meal, or oleic acid, by an indirect mechanism triggered in the proximal bowel, using nicotinic synapses, and involving nitric oxide release for PYY and an unknown mediator for PGDPs. For PYY there is a later phase of peptide release, probably induced by direct contact between nutrients and colonic L-cells.
We assessed the association of body mass and gastric volumes (fasting and postprandial) with satiation and postprandial symptoms.
Healthy obese and nonobese subjects underwent measurement of caloric intake at maximum satiation; postprandial symptoms were measured with visual analogue scales 30 minutes after a meal. Gastric volume during fasting and after 300 mL of Ensure was measured with technetium-99m single-photon emission computed tomography imaging. We used multiple regression analysis to assess the associations among variables.
Among 134 participants (81 women and 53 men), the median age was 26 years (range, 12-58 years), and the median body mass index was 24 kg/m(2) (range, 17-48 kg/m(2)). Increased body mass index, but not height, was associated with delayed satiation (P < 0.003, adjusted for sex). Overweight and obese subjects ingested, on average, 225 +/- 57 more kilocalories (945 +/- 239 kJ) at maximum satiation compared with normal weight individuals. Increased fasting gastric volume was not associated with body mass index or height, but it was significantly associated with delayed satiation (P = 0.001, adjusted for body mass index and sex). An increase of 50 mL in the fasting gastric volume was associated with 114 +/- 32 kcal (479 +/- 134 kJ) more ingested at maximum satiation. Increased body mass index was associated with lower fullness scores 30 minutes after a meal (P = 0.0012, adjusted for sex and volume of Ensure ingested). In contrast, scores of postprandial bloating and pain were higher with increased body mass index (both P < 0.05, adjusted for sex and volume of Ensure ingested).
Greater body mass index and fasting gastric volume are associated with reduced satiation. Increased body mass index or height was not associated with greater gastric volumes.
Fatty acid oxidation is thought to play a role in the control of food intake, and a low postprandial oxidation of ingested fat may contribute to the overeating on a high-fat diet. Evidence for a role of fatty acid oxidation in control of food intake is mainly derived from the stimulation of feeding in response to administration of the acyl-CoA-dehydrogenase inhibitor mercaptoacetate (MA) and other inhibitors of fatty acid oxidation in different species (rat, mouse, man). Denervation studies suggest that this "lipoprivic feeding" is related to changes in hepatic fatty acid oxidation. In contrast to the strong case for a feeding stimulatory effect of an inhibition of fatty acid oxidation, the evidence for a feeding suppressive effect of a stimulation of fatty acid oxidation is inconsistent and comparatively weak. Ingestion of medium-chain fatty acids (MCFA) and peripheral administration of substances known to increase fatty acid oxidation, such as the fatty acid synthase inhibitor C75 and beta3-adrenergic agonists, decrease feeding. Yet, these substances also reduce the rats' usual preference for saccharin solution, indicating that the feeding suppressive effect is not only due to a stimulation of fatty acid oxidation. A possible approach to answer the question of whether a stimulation of hepatic fatty acid oxidation enhances satiety is to selectively increase expression and activity of the enzyme CPT 1alpha in the liver. CPT 1alpha transfers long-chain fatty acids in the cytosol from CoA to carnitine, which is the precondition for the entry of long-chain fatty acids into mitochondria and the rate-controlling step in mitochondrial fatty acid oxidation. The generation of rats with inducible, liver-specific overexpression of CPT 1alpha should permit to critically examine the putative contribution of hepatic fatty acid oxidation to the control of food intake.
Glucagon-like peptide 1 (GLP-1) is a gut hormone that decreases appetite and promotes satiety. Its role in energy metabolism regulation is still poorly understood.
The aim of the study was to investigate the relation of fasting plasma GLP-1 concentrations to rates of energy expenditure (EE) and substrate oxidation-ie, respiratory quotient (RQ).
Forty-six glucose-tolerant white subjects (22 men, 24 women) aged 18-49 y whose adiposity spanned a wide range [body mass index (in kg/m2): 18.5-50] were studied in an inpatient clinic. Main outcome measures included resting EE and RQ (ventilated hood technique), body composition (dual-energy X-ray absorptiometry), and fasting plasma concentrations of GLP-1, pancreatic polypeptide, glucose, and insulin.
Fasting plasma GLP-1 concentrations were positively associated with resting EE (after adjustment for age, sex, and body composition) and negatively correlated with RQ (after adjustment for age, sex, and percentage body fat) and fasting plasma pancreatic polypeptide concentrations (both before and after adjustment for age, sex, percentage body fat, and fasting plasma glucose and insulin concentrations). Adjustment for fasting plasma pancreatic polypeptide concentrations, a marker of parasympathetic outflow to the gut, attenuated the strength of the association of fasting plasma GLP-1 concentrations with resting EE and RQ.
Higher fasting plasma GLP-1 concentrations are associated with higher rates of EE and fat oxidation independent of age, sex, and body composition. The autonomic nervous system may have a role in this relation. This effect, along with the established role of GLP-1 in promoting satiety, may further foster its therapeutic potential in the treatment of obesity.
Obesity is the most common form of malnutrition in pets, affecting more than one third of adult dogs and cats in developed countries. Obesity may be considered a disease itself because it is an inflammatory condition as well as a significant risk factor for other diseases. Diagnosis in pets is made earlier via routine use of a body condition scoring system. Management involves decreasing calorie intake and increasing calorie expenditure. Nutrient-modified diets can help when fed appropriately. Prevention and management of obesity involve early and frequent client counseling regarding suitable feeding management.
The management of anorexia should center first on the urgent and emergent medical management of the patient and be followed by feeding of a highly palatable food in a low-stress environment and manner. Diet palatability can potentially be improved by increasing dietary moisture, fat, or protein, and, in the dog, by adding sugar or salt as well as by using a variety of fresh, pleasantly aromatic, and uncommon foods. Caution should be used when increasing or adding nutrients that may be harmful to patients with specific diseases. Concurrent drug therapy that may reduce appetite should be minimized, and physical barriers to eating should be removed. Patients that consume less than resting energy requirement of longer than 3 to 5 days with no trend toward improving should receive parenteral or enteral nutrition.