F Santini

Università di Pisa, Pisa, Tuscany, Italy

Are you F Santini?

Claim your profile

Publications (142)561.68 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Modern treatment of type 2 diabetes must rely on therapy individualization. Morbid obesity confers an independent excess of risk to diabetes. In these individuals metabolic surgery is an opportunity the physician should consider, especially at the time of the diagnosis of diabetes, because of its efficacy and long-term effects. Besides the possible remission of diabetes, bariatric surgery is also associated with reduced risk of micro and macrovascular complications. A multidisciplinary team approach is necessary to maximize the beneficial effects and minimize the adverse events of metabolic surgery and to ensure proper follow-up based on the residual possibility of developing complications. In this regard, a consensus on definition of remission must be reached to define the residual risk after anti-diabetic drug withdrawal. Finally, randomized clinical trials are deemed necessary to establish risk-to-benefit profile of glucose-lowering agents for those patients who have remained diabetic or experience a disease relapse.
    No preview · Article · Feb 2016 · Surgery for Obesity and Related Diseases
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The use of angiotensin-converting enzyme inhibitors (ACE-I) and angiotensin II receptor blockers (ARB) for the treatment of hypertensive obese patients is steadily increasing. Some studies have reported that the use of these drugs was associated with an increased risk of hypotensive episodes, during general anaesthesia. The number of bariatric procedures is also increasing worldwide, but there is a lack of studies investigating the hypotensive effect of renin-angiotensin system (RAS) blockers in severely obese patients during general anaesthesia for bariatric surgery. The aim of this pilot study was to evaluate hemodynamic changes induced by general anaesthesia in obese patients chronically treated with ACE-I or ARB compared to a control group not treated with antihypertensive therapy. Fourteen obese subjects (mean body mass index (BMI) 47.5 kg/m(2)) treated with ACE-I or ARB and twelve obese (mean BMI 45.7 kg/m2) controls not treated with antihypertensive therapy underwent general anaesthesia to perform laparoscopic bariatric surgery. Systolic blood pressure, diastolic blood pressure, and heart rate were monitored continuously and registered at different time points: T0 before induction, then at 2, 5, 7, 10, 15, 20, 30, 60, 90, 120, and 150 min after induction, and the last time point taken following recovery from anaesthesia. A progressive reduction of both systolic and diastolic blood pressure values was observed without significant differences between the two groups. A similar trend of heart rate values was observed. In conclusion, our pilot study suggests that RAS blockers may be continued during the perioperative period in patients undergoing bariatric surgery, without increasing the risk of hypotensive episodes.
    Full-text · Article · Sep 2015 · Obesity Surgery
  • [Show abstract] [Hide abstract]
    ABSTRACT: Eating dyscontrol constitutes a potential negative predictor for the outcome of treatment strategies for obese patients. The aim of this study was to examine the qualitative characteristics of eating dyscontrol in obese patients who engage in binge eating (BE) compared with those who do not (NBE), and to analyse the relationship between eating dyscontrol and axis-I, axis-II, spectrum psychopathology using instruments that explore mood, panic-agoraphobic, social-phobic, obsessive-compulsive and eating disorders spectrum psychopathology (SCI-MOODS-SR, SCI-PAS-SR, SCI-SHY-SR, SCI-OBS-SR, SCI-ABS-SR). This was a cross-sectional study involving a clinical sample of adult obese patients with severe obesity (average body mass index = 45 ± 8 kg m(-2) ) and candidate to bariatric surgery who were recruited between November 2001 and November 2010 at the Obesity Center of the Endocrinology Unit, University Hospital of Pisa. All participants completed a face-to-face interview, including a diagnostic assessment of axes-I and II mental disorders (using the Structured Clinical Interview for Manual of Mental Disorders, fourth edition [SCID]-I and SCID-II) and filled out self-report spectrum instruments. Among obese patients not affected by BE, eating dyscontrol was highly represented. Indeed, 39.7% (N = 177) of subjects endorsed six or more items of the Anorexia-Bulimia Spectrum Self-Report, lifetime version domain exploring this behaviour. The cumulative probability of having axis-I, axis-II and a spectrum condition disorder increased significantly with the number of eating dyscontrol items endorsed. In both BE and NBE obese subjects, eating dyscontrol may represent an independent dimension strongly related to the spectrum psychopathology and axes I/II disorders. A systematic screening for eating dyscontrol symptoms by means of self-report spectrum instruments may be valuable to assign specific treatment strategies. © 2015 World Obesity.
    No preview · Article · Feb 2015
  • Giovanni Ceccarini · Alessio Basolo · Ferruccio Santini
    [Show abstract] [Hide abstract]
    ABSTRACT: A reciprocal interaction between the hypothalamo-pituitary-thyroid axis and the adipose tissue is required for the proper homeostasis of energy balance. In this chapter, the mechanisms by which the two systems regulate each other and the effects of thyroid dysfunctions on body weight will be discussed. In both lean and obese subjects, thyroid hormone and TSH levels are strongly influenced by the individual nutritional status. Furthermore, obesity can be associated with variations of circulating thyroid hormone and TSH. Whether obesity is a risk factor for thyroid diseases (autoimmunity, nodularity, cancer) remains a matter of debated investigation. While the hormonal substitutive treatment is required when obesity is associated with subclinical or overt hypothyroidism, we do not recommend thyroid hormone treatment in case of the isolated hyper-thyrotropinemia often detected in obese patients. Historically, many attempts have been carried out to treat obese euthyroid subjects by administration of thyroid hormones, their analogues, or derivatives, with the aim of increasing energy expenditure and promoting weight loss, but at present such type of intervention is not advisable outside very well-controlled clinical trials.
    No preview · Article · Jan 2015
  • G Ceccarini · M Maffei · P Vitti · F Santini
    [Show abstract] [Hide abstract]
    ABSTRACT: While it is now accepted that genes and their products affect food intake, the concept that locomotor behavior or the propensity for physical activity is controlled by neuro hum oral regulators is frequently underappreciated. In mammals, complex interactions have developed to allow the cross-talk between fuel homeostasis and physical activity. The aim of this review is to provide a synopsis of the influence of the leptin-melanocortin pathway, a well-studied pivotal player in body weight regulation, on locomotor behaviors. In rodents, reductions in leptin levels that physiologically occur following acute food deprivation or a reduction of the fat mass consequent to prolonged caloric restrictions are associated with a decrease in total locomotor activity and simultaneous increase in food-anticipatory activity, a locomotor behavior which reflects a foraging attitude. These actions can be prevented by leptin administration and are at least partially mediated by the neurons of the melanocortin pathway. In humans, twin studies have attributed to genetic factors approximately 50 % of the variance of physical activity. An elevated number of the genes or loci which may affect physical activity are involved in body weight homeostasis. Polymorphisms of the melanocortin-4 and leptin receptors have repeatedly been associated with the level of physical activity. Unraveling the complexity of the regulation of locomotor behavior and the interconnections with the pathways involved in energy homeostasis may help explain the substantial individual variability in physical activities in humans and disentangle the harmful effects of sedentary lifestyle, which may be distinct from the detrimental effects of obesity.
    No preview · Article · Dec 2014 · Journal of endocrinological investigation
  • [Show abstract] [Hide abstract]
    ABSTRACT: Objective Progressive lipodystrophy is one of the major features of the rare MDPL syndrome. Until now, 9 patients affected by this syndrome have been described and a recent study identified in 4 of them an in-frame deletion (Ser605del) of a single codon in the POLD1 gene. Sequence alterations of the POLD1 gene at different sites have been previously reported in human colorectal and endometrial carcinomas. Materials/Methods A 48-year-old woman was admitted to our Department for the assessment of a previously diagnosed lipodystrophy. She did not report a family history of diabetes or other metabolic disorders. Hypertriglyceridemia was diagnosed incidentally when she was 25 years old. At that time she was also diagnosed with sensorineural bilateral hearing loss. At physical examination she presented lipoatrophy affecting nearly the entire body, mandibular hypoplasia, bird-like face, beaked nose, progeroid facial features, with crowded teeth, small mouth and uvula. Abdominal ultrasound showed hepatomegaly and hepatosteatosis. Fat Mass Index measured with DXA was 4.59 Kg/m2, indicating a fat deficit; the oral glucose tolerance test showed an impaired glucose tolerance. Results Sequence analysis of the entire coding region of the POLD1 gene, disclosed a novel heterozygous mutation in exon 13 (R507C). Conclusion The MDPL patient herein described harbors a novel mutation in the exonuclease domain of POLD1. This new variant provides further evidence for a role of POLD1 in the pathogenesis of MDPL. The mechanisms that link changes at various sites of the protein with different diseases remain to be clarified.
    No preview · Article · Nov 2014 · Metabolism
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Obesity and thyroid diseases are common disorders in the general population and they frequently occur in single individuals. Alongside a chance association, a direct relationship between 'thyroid and obesity' has been hypothesized. Thyroid hormone is an important determinant of energy expenditure and contributes to appetite regulation, while hormones and cytokines from the adipose tissue act on the CNS to inform on the quantity of energy stores. A continuous interaction between the thyroid hormone and regulatory mechanisms localized in adipose tissue and brain is important for human body weight control and maintenance of optimal energy balance. Whether obesity has a pathogenic role in thyroid disease remains largely a matter of investigation. This review highlights the complexity in the identification of thyroid hormone deficiency in obese patients. Regardless of the importance of treating subclinical and overt hypothyroidism, at present there is no evidence to recommend pharmacological correction of the isolated hyperthyrotropinemia often encountered in obese patients. While thyroid hormones are not indicated as anti-obesity drugs, preclinical studies suggest that thyromimetic drugs, by targeting selected receptors, might be useful in the treatment of obesity and dyslipidemia.
    Preview · Article · Oct 2014 · European Journal of Endocrinology
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background Oxidative stress (OS) plays a major role on tissue function. Several catabolic or stress conditions exacerbate OS, inducing organ deterioration. Haptoglobin (Hp) is a circulating acute phase protein, produced by liver and adipose tissue, and has an important anti-oxidant function. Hp is induced in pro-oxidative conditions such as systemic inflammation or obesity. The role of systemic factors that modulate oxidative stress inside muscle cells is still poorly investigated. Results We used Hp knockout mice (Hp-/-) to determine the role of this protein and therefore, of systemic OS in maintenance of muscle mass and function. Absence of Hp caused muscle atrophy and weakness due to activation of an atrophy program. When animals were stressed by acute exercise or by high fat diet (HFD), OS, muscle atrophy and force drop were exacerbated in Hp-/-. Depending from the stress condition, autophagy-lysosome and ubiquitin-proteasome systems were differently induced. Conclusions Hp is required to prevent OS and the activation of pathways leading to muscle atrophy and weakness in normal condition and upon metabolic challenges.
    Full-text · Article · Jun 2014 · PLoS ONE
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Aim: Aim of this study was to validate the Comprehensive Appropriateness Scale for the Care of Obesity in Rehabilitation (CASCO-R) and to determine the cut-off score for indicating the most appropriate health care setting for patients with obesity. Methods: The CASCO-R scale was developed according to the available scientific literature and expertise of an expert panel working for a Consensus document endorsed by the Italian Society of Obesity (SIO) and the Italian Society for the Study of Eating Disorders (SISDCA). 16 Italian centres, specialized in the treatment of obesity, characterised by different settings of care (specialist outpatient service, day-hospital service, intensive inpatient rehabilitation), participated in the study. Results: 449 obese subjects were enrolled in the study (30.5% males and 69.5% females): 38.3% from outpatient services, 20.7% from day-hospital services and 40.9% from intensive inpatient rehabilitation units. After 2-month of treatment, a workload summary sheet, including medical and nursing interventions, number of expert advices and diagnostic procedures, and adverse clinical events (ACEs) was fulfilled for each patient. Statistically significant correlation was found between the CASCO-R scale score, overall workload and ACEs. The CASCO-R scale demonstrated also an excellent performance in terms of internal validity and test-retest analysis. Three total score cut-off have been proposed: >25 for inpatient intensive rehabilitation; 20-25 for day-hospital service; <20 for outpatient treatment. Conclusions: In conclusion, the CASCO-R scale was demonstrated to be a valid tool for assessing the appropriateness of the choice of the level of care. Hence, it can be used to verify the proper allocation of patients, as it was well correlated with measures of workload and the incidence of ACEs.
    Full-text · Article · May 2014 · Annali di igiene: medicina preventiva e di comunità
  • [Show abstract] [Hide abstract]
    ABSTRACT: Objective: Sulfate conjugation of thyroid hormones is an alternate metabolic pathway that facilitates the biliary and urinary excretion of iodothyronines and enhances their deiodination rate, leading to the generation of inactive metabolites. A de-sulfating pathway reverses this process and thyromimetic effects have been observed following the parenteral administration of 3,5,3'-triiodothyronine sulfate (T3S) in rats. The present study investigated whether T3S is absorbed after oral administration in humans and if it represents a source of 3,5,3'-triiodothyronine (T3).Methods: Twenty-eight hypothyroid patients (7 men and 21 women, mean age ± SD = 44 ± 11 years) who had a thyroidectomy for thyroid carcinoma were enrolled. Replacement thyroid hormone therapy was withdrawn (42 days for thyroxine, 14 days for T3) prior to radioiodine remnant ablation. A single oral dose of 20, 40, 80 (4 patients/group) or 160 μg (16 patients/group) T3S was administered 3 days before the planned administration of 131I. Blood samples for serum T3S and total T3 (TT3) concentrations were obtained at various times up to 48 hours after T3S administration.Results: At all T3S doses, serum T3S concentrations increased reaching a peak at 2-4 hours and progressively returned to basal levels within 8 to 24 h. The T3S Cmax and area under the curve (AUC0-48h) were directly and significantly related to the administered dose.An increase in serum TT3 concentration levels was observed, significant after 1 hour, further increased at 2 and 4 hours, and then remained steady up to 48 hours after T3S administration. There was a significant direct correlation between the TT3 AUC0-48h and the administered dose of T3S. No changes in serum free thyroxine (FT4) concentrations during the entire study period were observed, while serum TSH levels increased slightly at 48 hours not related to the dose of administered T3S. No adverse events were reported.Conclusions: 1) T3S is absorbed following oral administration in hypothyroid humans; 2) the oral administration of a single dose of T3S is converted to T3 in a dose-dependent manner and results in steady state serum T3 concentrations for 48 hours; 3) T3S may represent a new agent in combination with thyroxine (T4) in the therapy of hypothyroidism, if similar conversion of T3S to T3 can be demonstrated in euthyroid patients who are already taking T4.
    No preview · Article · Feb 2014 · Endocrine Practice
  • [Show abstract] [Hide abstract]
    ABSTRACT: Hepatitis C virus infection and diabetes mellitus are two worldwide, major public health problems with increasing complication and mortality rates. Type 1 diabetes mellitus (T1D) is characterized by an autoimmune process leading to pancreatic beta cell destruction; only when the major part of pancreatic beta cells have been destroyed the diabetes become clinically manifest. At the basis of the development of the T1D there is an interplay among environmental factors, pancreatic beta cells, the innate and adaptive immune system, the genetic background and the comorbidities of the patient. Viral infections, including hepatitis C virus infection, may be one of the factors that can almost accelerate progression to diabetes, through different mechanisms.
    No preview · Article · Nov 2013 · La Clinica terapeutica
  • [Show abstract] [Hide abstract]
    ABSTRACT: Obesity has reached global epidemic proportions and has been associated with numerous comorbidities, including major cardiovascular diseases and heart failure. It has many adverse effects on hemodynamics and cardiovascular structure and function; it increases total blood volume and cardiac output, and also activates several neurohumoral systems that play an important role in causing cardiac dysfunction. Typically, obese patients have a higher cardiac output but a lower level of total peripheral resistance at any given level of arterial pressure. Over the past few years, experimental evidence has unraveled some important pathogenetic mechanisms that may underlie a specific form of "obesity cardiomyopathy". However, many unanswered questions remain regarding the pathophysiological interactions between obesity and the heart.
    No preview · Article · Nov 2013 · Heart and Metabolism
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Serotonin (5-HT) is a well-known modulator of eating behavior. However, the molecular mechanisms linking its action to body weight balance have been only partially elucidated. Since platelets are a suitable peripheral model to study 5-HT transport, metabolism and release, we herein evaluated the expression of the platelet 5-HT re-uptake system (SERT) by [3H]-paroxetine binding assay. A cohort of 114 unrelated individuals (34 males, 80 females; age, mean +/- SD: 38.57 +/- 12.47 years) without major psychiatric disorders, was recruited following a naturalistic design regarding age or gender and classified accordingly to their body mass index (BMI). Subjects were divided into 5 groups: normal-weight (NW), overweight (OW) and grade I-III obese (OB) individuals. For gender analyses, data were transformed into [3H]-paroxetine density (Bmax)/BMI ratios to overcome both the disparity of women vs. men number and anthropometric differences between sexes. [3H]-paroxetine Bmax (SERT density, fmol/mg proteins) was reduced in platelet membranes of grade II (p < 0.01) and III (p < 0.001) obese subjects vs. controls and in overweight subjects (p < 0.05) vs. grade III obese individuals. Considering all patients together, a strong negative correlation between Bmax and BMI (r = -0.449; P < 0.0001) was demonstrated. Conversely, [3H]-paroxetine KD (dissociation constant, nM) did not differ among groups. No gender-related variation concerning Bmax/BMI ratios was observed in this cohort of subjects. The down-regulation of SERT in platelet membranes of severe human obesity (BMI > 35 Kg/m2) confirms the involvement of 5-HT system in body weight gain. Moreover, this findings may help to elucidate those monoamine-endocrine networks acting on fat storage, adipocyte signaling and energy balance. Targeting 5-HT/5-HT-related markers will possibly uncover the existence of human obesity subtypes.
    Full-text · Article · Oct 2013 · BMC Neuroscience
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The prevalence of severe obesity, defined as body mass index (BMI) ≥35.0 kg/m2, is rising rapidly. Given the disproportionately high health burden and healthcare costs associated with this condition, understanding the underlying aetiology, including predisposing genetic factors, is a biomedical research priority. Previous studies have suggested that severe obesity represents an extreme tail of the population BMI variation, reflecting shared genetic factors operating across the spectrum. Here, we sought to determine whether a panel of 32 known common obesity-susceptibility variants contribute to severe obesity in patients (n = 1,003, mean BMI 48.4±8.1 kg/m2) attending bariatric surgery clinics in two European centres. We examined the effects of these 32 common variants on obesity risk and BMI, both as individual markers and in combination as a genetic risk score, in a comparison with normal-weight controls (n = 1,809, BMI 18.0–24.9 kg/m2); an approach which, to our knowledge, has not been previously undertaken in the setting of a bariatric clinic. We found strong associations with severe obesity for SNP rs9939609 within the FTO gene (P = 9.3×10−8) and SNP rs2815752 near the NEGR1 gene (P = 3.6×10−4), and directionally consistent nominal associations (P<0.05) for 12 other SNPs. The genetic risk score associated with severe obesity (P = 8.3×10−11) but, within the bariatric cohort, this score did not associate with BMI itself (P = 0.264). Our results show significant effects of individual BMI-associated common variants within a relatively small sample size of bariatric patients. Furthermore, the burden of such low-penetrant risk alleles contributes to severe obesity in this population. Our findings support that severe obesity observed in bariatric patients represents an extreme tail of the population BMI variation. Moreover, future genetic studies focused on bariatric patients may provide valuable insights into the pathogenesis of obesity at a population level.
    Full-text · Article · Aug 2013 · PLoS ONE
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background: Left Ventricular Diastolic Dysfunction (LVDD) represents one of the cardiac consequences in overweight and obese patients. Resting heart rate (RHR) is an easy measure but important indicator of cardiovascular health. In this study, we sought to assess if RHR is a reliable determinants of LVDD in obese patients with or without arterial hypertension. Methods and results: A perspective echo-Doppler study was performed in 154 consecutive asymptomatic patients with grade 1-to-3 obesity (body mass index [BMI]: 43±8) who averaged 47 years in age (women 80%). All patients had a LV ejection fraction (EF) ≥50% and no history of heart failure or coronary artery disease. LVDD was identified by an E/A ratio >1.5 and an E/A ratio <0.8. Long-axis function was assessed by global longitudinal strain. For means of comparison, 56 age-matched subjects with or without hypertension were also studied. Prevalence of hypertension was 42% in obese patients, while it was 29% in the control group. LVDD was present in 46 obese patients (30%) and in 12 controls (21%). Patients with grade 3 obesity (BMI ≥40) exhibited higher LV volumes and mass (p<0.0001), cardiac output (p<0.0001), left atrial size (p<0.0001), stroke volume (p<0.0001) and RHR (p<0.0001), and a worse LV long-axis function (p<0.001) as compared to patients with grade 1-2 obesity (BMI between 30 and 40) and the control group. In patients with grade 2-to-3 obesity, BMI directly correlated with stroke volume (r=0.24; p=0.003) and cardiac output (r=0.37; p<0.0001), RHR inversely correlated with LV end-diastolic volume index (r=-0.48; p<0.0001), LV end-systolic volume index (r=-0.42; p<0.0001) and LV mass index (r=-0.40; p<0.0001). RHR (hazard ratio [HR]:1.06, p=0.003) and age (HR: 1.05, p=0.025) were independently associated with LVDD in patients with grade 2-to-3 obesity. Conclusion: In obese patients with or without hypertension, RHR was a major predictor of LVDD and negatively correlated with LV mass and volumes. Obese patients with a disproportionate increase in RHR are likely to carry inadequate allometric scaling of LV mass and volumes relative to their BMI values.
    Preview · Article · Aug 2013 · European Heart Journal
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Mutations in the coding sequence of the X-linked gene MeCP2 (Methyl CpG-binding protein) are present in around 80% of patients with Rett Syndrome, a common cause of intellectual disability in female and to date without any effective pharmacological treatment. A relevant, and so far unexplored feature of RTT patients, is a marked reduction in peripheral circulation. To investigate the relationship between loss of MeCP2 and this clinical aspect, we used the MeCP2 null mouse model B6.129SF1-MeCP2tm1Jae for functional and pharmacological studies. Functional experiments were performed on isolated resistance mesenteric vessels, mounted on a pressurized myograph. Vessels from female MeCP2(+/-) mice show a reduced endothelium-dependent relaxation, due to a reduced Nitric Oxide (NO) availability secondary to an increased Reactive Oxygen Species (ROS) generation. Such functional aspects are associated with an intravascular increase in superoxide anion production, and a decreased vascular eNOS expression. These alterations are reversed by curcumin administration (5% (w/w) dietary curcumin for 21 days), which restores endothelial NO availability, decreases intravascular ROS production and normalizes vascular eNOS gene expression. In conclusion our findings highlight alterations in the vascular/endothelial system in the absence of a correct function of MeCP2, and uncover related cellular/molecular mechanisms that are rescued by an anti-oxidant treatment.
    Full-text · Article · May 2013 · PLoS ONE
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: GPR7, the endogenous coupled receptor for neuropeptide B and neuropeptide W, is expressed in several regions of the Central Nervous System (CNS), which are involved in the regulation of feeding behaviour. GPR7 affects the regulation of energy balance through a mechanism independent of leptin and melanocortin pathways. Aim: Aim of this study was to investigate whether GPR7 gene mutations can be detected in human subjects and, in that event, if they are differently distributed among lean and obese subjects. Subjects and Methods: The coding region of GPR7 were sequenced in 150 obese patients and 100 normal-weight unrelated controls. Functional studies of the allelic variants were performed. Results: One genetic GPR7 variant was found (Tyr135Phe - rs33977775) in obese subjects (13,3%) and lean control (25%). Functional studies did not reveal significant differences between the wild type and the Tyr135Phe allelic variants in their NPW mediated capacity to inhibit forskolin-induced cAMP production. Conclusions: Screening of GPR7 gene mutations among lean and obese subjects revealed a Tyr135Phe allelic variant that was fairly common in the study population. As indicated by in vitro and in silico studies, this variant is unlikely to cause a functional derangement of the receptor.
    No preview · Article · Apr 2013 · Journal of endocrinological investigation
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background:Short sleep and weight gain are inversely related. Sleep deprivation acutely increases food intake but little is known about eating behavior in chronically sleep-deprived, obese individuals.Objective:To characterize the relationship between sleep, food intake and alcohol consumption under free-living conditions in obese, chronically sleep-deprived individuals.Design:Cross-sectional study of a cohort of obese men and premenopausal women.Subjects:A total of 118 obese subjects (age: 40.3±6.7 years; 91 females/27 males; body mass index 38.7±6.4 kg m(-2)).Measurements:Energy, macronutrient, alcohol and caffeine intake assessed by 3-day food records. Sleep duration estimated by actigraphy. Respiratory disturbance index assessed by a portable device.Results:Subjects slept 360.7±50.2 min per night and had a total energy intake of 2279.1±689 kcal per day. Sleep duration and energy intake were inversely related (r=-0.230, P=0.015). By extrapolation, each 30-min deficit per day in sleep duration would translate to an ∼83 kcal per day increase in energy intake. In addition, sleep apnea was associated with a shift from carbohydrate to fat intake. Alcohol intake in subjects consuming >3.5 g of alcohol per day (N=41) was inversely related to sleep duration (r=-0.472, P=0.002).Conclusions:Shorter sleep duration and obstructive sleep apnea are associated with higher energy, fat and alcohol intakes in obese individuals. The importance of this study relies on the population studied, obese subjects with chronic sleep deprivation. These novel findings apply to the large segment of the US population who are obese and sleep-deprived.
    Full-text · Article · Jan 2013 · Nutrition & Diabetes
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background:Short sleep and weight gain are inversely related. Sleep deprivation acutely increases food intake but little is known about eating behavior in chronically sleep-deprived, obese individuals.Objective:To characterize the relationship between sleep, food intake and alcohol consumption under free-living conditions in obese, chronically sleep-deprived individuals.Design:Cross-sectional study of a cohort of obese men and premenopausal women.Subjects:A total of 118 obese subjects (age: 40.3±6.7 years; 91 females/27 males; body mass index 38.7±6.4 kg m(-2)).Measurements:Energy, macronutrient, alcohol and caffeine intake assessed by 3-day food records. Sleep duration estimated by actigraphy. Respiratory disturbance index assessed by a portable device.Results:Subjects slept 360.7±50.2 min per night and had a total energy intake of 2279.1±689 kcal per day. Sleep duration and energy intake were inversely related (r=-0.230, P=0.015). By extrapolation, each 30-min deficit per day in sleep duration would translate to an ∼83 kcal per day increase in energy intake. In addition, sleep apnea was associated with a shift from carbohydrate to fat intake. Alcohol intake in subjects consuming >3.5 g of alcohol per day (N=41) was inversely related to sleep duration (r=-0.472, P=0.002).Conclusions:Shorter sleep duration and obstructive sleep apnea are associated with higher energy, fat and alcohol intakes in obese individuals. The importance of this study relies on the population studied, obese subjects with chronic sleep deprivation. These novel findings apply to the large segment of the US population who are obese and sleep-deprived.
    Full-text · Article · Jan 2013
  • Source

    Full-text · Dataset · Nov 2012

Publication Stats

3k Citations
561.68 Total Impact Points

Institutions

  • 1987-2015
    • Università di Pisa
      • • Department of Clinical and Experimental Medicine
      • • Department of Chemistry and Industrial Chemistry
      Pisa, Tuscany, Italy
  • 2006
    • Azienda Ospedaliero-Universitaria Pisana
      Pisa, Tuscany, Italy
  • 2001
    • Università degli studi di Parma
      Parma, Emilia-Romagna, Italy
  • 1995
    • Long Beach Memorial Medical Center
      Long Beach, California, United States
  • 1992-1994
    • University of California, Los Angeles
      • • Division of Endocrinology
      • • Department of Medicine
      Los Angeles, California, United States
  • 1993
    • California Health Sciences University
      Clovis, California, United States
  • 1989
    • Université Libre de Bruxelles
      Bruxelles, Brussels Capital, Belgium