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PubMed1986

Possible role of pancreatic insulin and glucagon in the hyperlipidemia and obesity of obese strain of chicken.

Circulating levels of insulin, glucagon, thyroid hormones as well as lipid levels were determined in an obese strain of chicken and their lean controls. Hepatic and muscle glycogen and lipids were also measured. Obese birds had higher plasma lipids accompanied by significantly higher insulin and lower glucagon levels compared to lean controls. Hepatic and muscle triglycerides were also higher in obese birds. Plasma T4 level was significantly higher in obese but T3 was not different in the two groups. Results suggest that genetically obese birds have significantly increased insulin/glucagon ratios as previously reported in the PTU induced hypothyroid-obese chicks (Horm. Metab. Res. 12: 51, 1980) and this could have causal relationship to hyperlipidemia and obesity observed in these birds.

Animals↗
PubMed1984

Decreased glucose-induced thermogenesis after weight loss in obese subjects: a predisposing factor for relapse of obesity?

Glucose-induced thermogenesis (GIT) after a 100-g oral glucose load was measured by continuous indirect calorimetry in 32 nondiabetic and diabetic obese subjects and compared to 17 young and 13 middle aged control subjects. The obese subjects were divided into three groups: A (n = 12) normal glucose tolerance, B (n = 13) impaired glucose tolerance, and C (n = 7) diabetics, and were studied before and after a body weight loss ranging from 9.6 to 33.5 kg consecutive to a 4 to 6 months hypocaloric diet. GIT, measured over 3 h and expressed as percentage of the energy content of the load, was significantly reduced in obese groups A and C (6.2 +/- 0.6, and 3.8 +/- 0.7%, respectively) when compared to their age-matched control groups: 8.6 +/- 0.7 (young) and 5.8 +/- 0.3% (middle aged). Obese group B had a GIT of 6.1 +/- 0.6% which was lower than that of the young control group but not different from the middle-aged control group. After weight loss, GIT in the obese was further reduced in groups A and B than before weight loss: ie, 3.4 +/- 0.6 (p less than 0.001), 3.7 +/- 0.5 (p less than 0.01) respectively, whereas in group C, weight loss induced no further diminution in GIT (3.8 +/- 0.6%). These results support the concept of a thermogenic defect after glucose ingestion in obese individuals which is not the consequence of their excess body weight but may be one of the factors favoring the relapse of obesity after weight loss.

Adult↗
PubMed1992

Left ventricular diastolic and systolic function in normotensive obese subjects: influence of degree and duration of obesity.

The present study was carried out to evaluate systolic and diastolic parameters in overweight and moderately obese, but otherwise healthy subjects, and in a lean control group, to determine whether degree and duration of obesity can influence left ventricular function. A total of 27 subjects, 17 overweight or with moderate obesity and 10 lean, healthy subjects were included. Patients were divided into three groups according to their body mass index (BMI) and to Garrow's criteria as follows: lean control group (BMI less than 25 kg.m-2); overweight subjects (BMI from 25 to 30 kg.m-2); moderately obese subjects (BMI greater than 30 less than 40 kg.m-2). Systolic and diastolic parameters were measured using blood pool gated radionuclide angiography. Left ventricular (LV) ejection fraction (EF), peak ejection rate (PER), time to PER (tPER), peak filling rate (PFR) and time to PFR (tPFR) were evaluated. PER and PFR values were normalized for end-diastolic volume (EDV). EF and PFR were significantly lower (P less than 0.05) both in moderately obese and in overweight subjects and tPFR was significantly (P less than 0.05) prolonged in both groups in comparison to lean controls. Only in moderately obese subjects was PER significantly (P less than 0.05) decreased and tPER significantly (P less than 0.05) prolonged in comparison to lean controls. As compared to overweight individuals, moderately obese subjects were characterized by a significant decrease (P less than 0.05) in LVEF and PER and by a significant increase (P less than 0.05) in tPER, without relevant change in PFR and in tPFR.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed2005

PON1 polymorphism, diabetes mellitus, obesity, and risk of myocardial infarction: Modifying effect of diabetes mellitus and obesity on the association between PON1 polymorphism and myocardial infarction.

PURPOSE: Previous studies on PON1 gene polymorphism and the risk of coronary atherosclerotic diseases have been inconsistent. This may be in part due to population difference in prevalence of high oxidative stress and its modifying effect on the association. Diabetes and obesity are two major risk factors of myocardial infarction (MI) and associated with high oxidative stress. We investigated the association between PON1 Q192R polymorphism and the risk of myocardial infarction (MI) and in particular, whether the association can be modified by diabetes mellitus (DM) and obesity. METHODS: We conducted a case-control study, including 154 MI cases and 154 controls enrolled in Beijing, China. Epidemiological and clinical data and PON1 Q192R genotype were obtained from each subject. RESULTS: Without considering the modifying effect of DM and obesity, PON1 Q192R polymorphism was not associated with MI. When simultaneously examining the joint association of this polymorphism, DM, and obesity with MI, as compared to subjects with QQ genotypes and without DM and obesity, subjects with QR/RR genotypes and with either DM or obesity had significantly higher risk of MI (OR = 3.6, 95% CI: 1.5-8.7). CONCLUSION: Our data suggest that PON1 Q192R polymorphism was not independently associated with MI but further increased the risk of MI among the subjects with DM, obesity, or both, the conditions associated with high oxidative stress.

Aryldialkylphosphatase↗
PubMed2006

Prevalence of gallbladder stone disease in obese children and adolescents: influence of the degree of obesity, sex, and pubertal development.

OBJECTIVES: The objective of the present study was to investigate the prevalence of gallbladder stone disease (GD) in a collective of obese children and adolescents and to assess the role of potential influencing factors such as the degree of obesity, sex, age, and pubertal development. METHODS: Four hundred ninety-three obese children and adolescents (body mass index standard deviation score [BMI-SDS] > 2.0p) aged 8 to 19 years (218 males, 275 females) were included in the study and underwent ultrasound for detection of GD. RESULTS: Gallbladder stones were detected in 10 of 493 (2.0%; 8 girls, 2 boys) subjects studied. None of the 95 prepubertal children examined were found to suffer from GD. Patients with GD were more severely obese (BMI-SDS 3.4 +/- 0.5 vs. 2.7 +/- 0.4; P < 0.001) and older (16.1 +/- 1.5 vs.13.9 +/- 2.0 years; P < 0.008) than children and adolescents without GD. CONCLUSIONS: Compared with published data for unselected children an adolescents, the prevalence of GD (2.0%) in obese children and adolescents, previously treated with diet for obesity, is high. Obesity and female sex appear even in children and adolescents to be risk factors for the development of GD. The occurrence of prepubertal GD is rare.

Adolescent↗
PubMed1998

Microsatellite marker content mapping of 12 candidate genes for obesity: assembly of seven obesity screening panels for automated genotyping.

Twin studies, adoption studies, and studies of familial aggregation indicate that obesity has a genetic component. Whereas, the genetic factors predisposing to obesity have been elucidated for several rare syndromes, the factors responsible for obesity in the general population have remained elusive. Genetic studies of complex traits are often accelerated by the use of candidate genes. To facilitate genetic studies of human obesity, seven multiplex panels of candidate genes for obesity that are suitable for fluorescent genotyping have been assembled. The multiplex panels are composed of 66 microsatellite markers linked tightly to 16 human gene products that are of potential importance in the control of body weight or linked to syndromic forms of obesity. As part of these efforts 12 previously cloned genes have been placed on the human physical map. In addition the chromosomal location of three of these genes, ART, NYP Y6R, and PPARgamma, are reported for the first time. These resources will be of use in studies to identify the genetic factors responsible for human obesity. [Figures are available at http://www.genome.org]

Agouti-Related Protein↗
PubMed2006

Gastroesophageal reflux disease in obese patients: the role of obesity in management.

Gastroesophageal reflux disease (GERD) is common in obese patients. The implications of obesity in the etiology, management and outcomes in treatment for GERD have become increasingly important due to an epidemic of obesity. The increasing prevalence of patients with both obesity and GERD merits evaluation of the appropriate surgical intervention for GERD and its symptoms. With the additional advantages of weight loss and resolution of weight-related morbidity (including GERD) bariatric procedures should be the procedure of choice in patients with medically complicated obesity. Patients in lower obesity classes with body mass indices (BMI) of 30-35 kg/m2 without other substantive weight-related comorbidity should prompt consideration of both fundoplication and bariatric procedures, tailoring the best approach based on the specific patient and future implications. Patients classified as overweight but not obese (BMI < 30) are likely best treated with fundoplication; however, no randomized trials comparing fundoplication with the current antireflux bariatric procedures exist.

Bariatric Surgery↗
PubMed1987

Leucocyte sodium pump activity after meals or insulin in normal and obese subjects: cause for increased energetic efficiency in obesity?

As cellular sodium pumping is an energy consuming process and differences in the obese may account for their energetic efficiency, leucocyte sodium-22 efflux was studied in obese and normal volunteers both in the fasting state and after a test meal or infusion of glucose and insulin intravenously. The 22Na ouabain sensitive efflux rate constant was significantly higher in obese subjects than normal (mean (1 SD) 2.69 (0.40)/h v 2.35 (0.49)/h). Two hours after a 4.2 MJ (1000 kcal) meal there was an increase in the efflux rate constant from its fasting value in normal weight subjects (2.39 (0.33)/h to 2.71 (0.40)/h) but not in obese subjects (2.65 (0.54)/h to 2.61 (0.58)/h). The rise in ouabain sensitive efflux rates was significantly higher in normal than obese subjects. Both groups showed a rise in intracellular sodium concentrations. The euglycaemic clamp produced similar results. Feeding or infusion of insulin increases sodium pump activity more in normal than obese subjects. This difference may contribute to any defective dietary thermogenesis in obesity, which may lead to energetic efficiency and a tendency to gain weight.

Adult↗
PubMed1983

Thermogenic drugs for the treatment of obesity: screening using obese rats and mice.

The thermogenic activity of ephedrine, ethinyloestradiol and triiodothyronine were compared by incorporating the drugs into the diets fed to groups of adult rats and mice. The animals used were normal lean mice, hypothalamic obese mice, dietary-induced obese mice and rats, and genetically obese mice and rats. Food intake and body weight were monitored throughout and oxygen consumption measurements were made. Finally, the animals were killed and their carcasses analysed. Generally, ethinyloestradiol reduced body weight by causing anorexia. Triiodothyronine increased oxygen consumption but also increased food intake such that in most cases body weight did not change; it killed the genetically obese animals, but reduced fat in the hypothalamic and dietary induced obese animals. The animals treated with ephedrine lost body weight and body fat without increasing food intake, and had elevated oxygen consumptions. This experiment not only demonstrated marked differences between the various laboratory animal models of obesity, but also that ephedrine is a potential slimming agent. It is relatively safe and has been used by us to obtain successful breeding using the genetically obese male animals which are normally sterile.

Animals↗
PubMed2006

Telmisartan prevents obesity and increases the expression of uncoupling protein 1 in diet-induced obese mice.

The aim of the present study was to clarify the effect of telmisartan, an angiotensin II receptor blocker, on the development of obesity and related metabolic disorders in diet-induced obese mice. Treatment with telmisartan dissolved in drinking water at a dosage of 5 mg/kg per day for 14 days attenuated the diet-induced weight gain without affecting food intake in diet-induced obese mice compared with controls using nontreated water. Telmisartan treatment decreased the weight of visceral adipose tissue and the triglyceride content in the liver and skeletal muscle. In addition, hyperglycemia, hyperinsulinemia, and hypertriglyceridemia in diet-induced obese mice all improved with telmisartan treatment. Furthermore, telmisartan treatment increased adiponectin mRNA in visceral white adipose tissue and was associated with a concomitant change in the serum adiponectin level. In contrast, the treatment reduced the serum level of resistin. Finally, telmisartan treatment increased the mRNA expression of uncoupling protein 1 in brown adipose tissue and was accompanied by an increase in oxygen consumption. In conclusion, telmisartan treatment might prevent the development of obesity and related metabolic disorders by altering the levels of adiponectin, resistin, and uncoupling protein 1 in diet-induced obese mice. Our results indicate that telmisartan can be used as a therapeutic tool for metabolic syndrome, including visceral obesity.

Adiponectin↗
PubMedDate not supplied

Relationship between cardiovascular risk indicators and types of obesity in overweight and obese women.

We aimed to evaluate the relationship between different types of obesity and cardiovascular risk indicators. A total of 623 overweight (body mass index [BMI] > 25 kg/m2), and 2559 obese (BMI > 30 kg/m2) women were divided into four groups according to their BMI and waist-to-hip ratio (WHR): simple overweight (BMI 25-30 kg/m2 and WHR < 0.8, n = 371), abdominal adiposity (BMI 25-30 kg/m2 and WHR > 0.8, n = 252), peripheral (pure) obesity (BMI > 30 kg/m2 and WHR < 0.8, n = 918) and central obesity (BMI > 30 kg/m2 and WHR > 0.8, n = 1641). The levels of the risk indicators measured (clinical, anthropometric and laboratory) were significantly higher in the central obesity group. Total body fat and abdominal fat accumulation seems to result in more serious hyperinsulinaemia and insulin resistance in central obesity. Measuring BMI and WHR in obese patients may reveal their risk for coronary heart disease.

Abdomen↗
PubMed2000

Understanding the role of glucocorticoids in obesity: tissue-specific alterations of corticosterone metabolism in obese Zucker rats.

The role of glucocorticoids in obesity is poorly understood. Observations in obese men suggest enhanced inactivation of cortisol by 5alpha-reductase and altered reactivation of cortisone to cortisol by 11betahydroxysteroid dehydrogenase type 1 (11betaHSD1). These changes in glucocorticoid metabolism may influence corticosteroid receptor activation and feedback regulation of the hypothalamic-pituitary-adrenal axis (HPA). We have compared corticosterone metabolism in vivo and in vitro in male obese and lean Zucker rats, aged 9 weeks (n = 8/group). Steroids were measured in 72-h urine and 0900 h trunk blood samples. 5alpha-Reductase type 1 and 11betaHSD activities were assessed in dissected tissues. Obese animals were hypercorticosteronemic and excreted more total corticosterone metabolites (2264+/-623 vs. 388+/-144 ng/72 h; P = 0.003), with a greater proportion being 5alpha-reduced or 11-oxidized. 11-Dehydrocorticosterone was also elevated in plasma (73+/-9 vs. 18+/-2 nM; P = 0.001) and urine (408+/-111 vs. <28 ng/72 h; P = 0.01). In liver of obese rats, 5alpha-reductase type 1 activity was greater (20.6+/-2.7% vs. 14.1+/-1.5%; P<0.04), but 11betaHSD1 activity (maximum velocity, 3.43+/-0.56 vs. 6.57+/-1.13 nmol/min/mg protein; P = 0.01) and messenger RNA levels (0.56+/-0.08 vs. 1.03+/-0.15; P = 0.02) were lower. In contrast, in obese rats, 11betaHSD1 activity was not different in skeletal muscle and sc fat and was higher in omental fat(36.4+/-6.2 vs. 19.2+/-6.6; P = 0.01), whereas 11betaHSD2 activity was higher in kidney (16.7+/-0.6% vs. 11.3+/-1.5%; p = 0.01). We conclude that greater inactivation of glucocorticoids by 5alpha-reductase in liver and 11betaHSD2 in kidney combined with impaired reactivation of glucocorticoids by 11betaHSD1 in liver may increase the MCR of glucocorticoids and decrease local glucocorticoid concentrations at these sites. By contrast, enhanced 11betaHSD1 in omental adipose tissue may increase local glucocorticoid receptor activation and promote obesity.

11-beta-Hydroxysteroid Dehydrogenase Type 1↗
PubMed2004

Relationship between serum resistin concentrations and insulin resistance in nonobese, obese, and obese diabetic subjects.

Early reports suggested that resistin is associated with obesity and insulin resistance in rodents. However, subsequent studies have not supported these findings. To our knowledge, the present study is the first assessment in human subjects of serum resistin and insulin sensitivity by the insulin clamp technique. Thirty-eight nonobese subjects [age, 23 +/- 4 yr; body mass index (BMI), 25.4 +/- 4.3 kg/m(2)], 12 obese subjects (age, 54 +/- 8 yr; BMI, 33.0 +/- 2.5 kg/m(2)), and 22 obese subjects with type 2 diabetes (age, 59 +/- 7 yr; BMI, 34.0 +/- 2.4 kg/m(2)) were studied. Serum resistin concentrations were not different among nonobese (4.1 +/- 1.7 ng/ml), obese (4.2 +/- 1.6 ng/ml), and obese diabetic subjects (3.7 +/- 1.2 ng/ml), and were not significantly correlated to glucose disposal rate during a hyperinsulinemic glucose clamp across groups. Serum resistin was, however, inversely related to insulin sensitivity in nonobese subjects only (r = -0.35; P = 0.05), although this association was lost after adjusting for percent body fat. Serum resistin was not related to percent fat, BMI, or fat cell size. A strong correlation was observed between serum resistin and resistin mRNA expression from abdominal sc adipose tissue in a separate group of obese subjects (r = 0.62; P < 0.01; n = 56). Although the exact function of resistin is unknown, we demonstrated only a weak relationship between resistin and insulin sensitivity in nonobese subjects, indicating that resistin is unlikely to be a major link between obesity and insulin resistance in humans.

Abdomen↗
PubMed2004

Race/ethnic issues in obesity and obesity-related comorbidities.

The prevalence of obesity is increasing among all age and racial groups in the United States. There is, however, a disproportionate rise in the prevalence of obesity among African-Americans and Hispanic/Mexican Americans. Obesity is a major contributor to the insulin resistant syndrome (IRS), a condition of multiple metabolic abnormalities that is a precursor to type 2 diabetes, and confers a high risk for cardiovascular events. The estimated prevalence of IRS is also greater in Mexican Americans and African-Americans than in Caucasians. The IRS is identifiable in children, and as with adults, there are racial differences in its expression even at a young age. The obesity-associated diseases, including diabetes and hypertension, are found at higher rates within the minority races compared with Caucasians. However, there are differences, in that obesity-related hypertension occurs at higher rates among African-Americans, and obesity-related diabetes occurs at higher rates among Mexican Americans. Race/ethnic differences in lifestyle behaviors and economic disadvantage may account for some of the race disparity in obesity-related diseases and disease outcomes. Environmental factors, however, do not explain all of the race disparity in disease expression, indicating that there are genetic/molecular factors that are operational as well.

Comorbidity↗
PubMed2005

Reversal of obesity-related hypoadiponectinemia by lifestyle intervention: a controlled, randomized study in obese adolescents.

CONTEXT: Hypoadiponectinemia and chronic subclinical inflammation in adults are associated with the development of diabetes and cardiovascular disease. The potential relationship between adiponectin and inflammation and its modulation by lifestyle intervention in the pediatric obese population remain unclear. OBJECTIVES: The objectives were to investigate in adolescents 1) the relationship between adiponectin and obesity-related inflammatory factors, C-reactive protein, and IL-6; and 2) the effect of a lifestyle intervention on adiponectin and whether these effects are related to changes in inflammatory factors. RESEARCH METHODS AND PROCEDURES: Twenty-one obese and age-matched lean adolescents (age, 14-18 yr; Tanner stage, > or =IV) were studied cross-sectionally. Fifteen obese adolescents also underwent a randomized, controlled physical activity-behavior-diet-based lifestyle intervention for 3 months. Associations among adiponectin, fat mass, insulin resistance, and inflammatory factors at baseline as well as after the intervention were assessed. RESULTS: Plasma adiponectin concentration was lower (P < 0.001) in the obese vs. age-matched lean adolescents. Significant inverse relationships were observed between adiponectin and inflammatory factors, insulinemia, insulin resistance, and fat mass. Intervention produced a 34% increase in adiponectin concentration (P = 0.0004) despite negligible weight loss but with reductions in fat mass, hyperinsulinemia, insulin resistance, and inflammatory factors (all P < 0.01). CONCLUSIONS: The data suggest that in adolescents, obesity-related hypoadiponectinemia is associated with subclinical inflammation, and a short-term lifestyle intervention augments adiponectin concentrations. These effects appear to be related to reductions in fat mass and inflammatory factors. Based on our current understanding of adiponectin physiology, reversal of hypoadiponectinemia in obese adolescents may protect against risks for cardiovascular disease and diabetes.

Adiponectin↗
PubMed2001

Does the laparoscopic approach significantly affect cardiac functions in laparoscopic surgery? Pilot study in non-obese and morbidly obese patients.

BACKGROUND: Laparoscopy in bariatric surgery represents a modern method generally associated with lower morbidity and mortality, compared with the traditional surgical approach. However, in patients with impaired cardiovascular function, the laparoscopic approach is limited by the potential adverse hemodynamic impact. We assessed the influence of some laparoscopic procedures on selected cardiac functions in significantly obese patients and in subjects with normal body weight, using transesophageal echocardiography (TEE). PATIENTS AND METHODS: Six subjects with normal body weight (mean BMI 25.3 +/- 3.6 kg/m2), and six patients undergoing laparoscopic gastric banding for morbid obesity (mean BMI 45.8 +/- 7.5 kg/m2) were studied. Heart rate (HR), blood pressure (BP), ejection fraction, cardiac output (CO) and transmitral flow were measured. Parameters were recorded at baseline before the operation (BL), after installation of capnoperitoneum (CP), and after positioning the patient for surgery (SP). RESULTS: Compared to BL, CP and SP were characterized by an increase in HR and BP in both groups of patients. As ejection fraction did not change significantly, the HR changes were accompanied by an increase in CO: (BL 5.8 +/- 2.2 l/min, CP 6.5 +/- 2.6 l/min, SP 6.7 +/- 2.7 l/min, p < 0.05 BL vs CP and SP). Transmitral flow parameters did not change significantly. Hemodynamic changes in subgroups with normal body build and in the obese patients were comparable. There was an increase in CO and pressure-rate product in obese individuals. CONCLUSIONS: Our results suggest that the hemodynamic response to laparoscopic surgery is characterized by an increase in CO (due to increased HR) and BP. In subjects without a manifest cardiovascular disease, neither systolic nor diastolic performance was significantly affected by the introduction of capnoperitoneum and positioning of the patient for surgery. Similar results were observed in obese and non-obese subjects. Phase II of this on-going study is focusing on impact and safety of laparoscopy in obese patients with known cardiovascular disease.

Adult↗
PubMed2005

Effects of metformin and ethinyl estradiol-cyproterone acetate on lipid levels in obese and non-obese women with polycystic ovary syndrome.

OBJECTIVE: Women with polycystic ovary syndrome (PCOS) exhibit risk factors for cardiovascular diseases such as abdominal obesity, insulin resistance and dyslipidemia. Insulin sensitizers, especially metformin, have been shown to improve these metabolic disturbances, but there are only a few studies on their effects on serum lipids in polycystic ovary syndrome. METHODS: Thirty-five women with PCOS (18 obese and 17 non-obese) were randomized to 6-month treatments with metformin or ethinyl estradiol-cyproterone acetate oral contraceptive pills. RESULTS: In the whole-study population (non-obese and obese women) serum levels of high-density lipoprotein cholesterol increased from 1.4+/-0.2 to 1.6+/-0.1 mmol/l (means +/-S.E. throughout) at 3 and 6 months (P < 0.001), the total cholesterol:high-density lipoprotein cholesterol ratio decreased significantly from 3.8+/-0.3 to 3.3+/-0.2 at 6 months (P < 0.001) and a similar trend was observed in serum triglyceride levels during metformin treatment. In the oral contraceptive group, serum levels of total cholesterol increased from 4.9+/-0.3 to 5.4+/-0.3 mmol/l (P < 0.05), high-density lipoprotein cholesterol increased from 1.2+/-0.1 to 1.5+/-0.1 mmol/l (P < 0.001), the total cholesterol:high-density lipoprotein cholesterol ratio decreased from 4.6+/-0.4 to 3.7+/-0.2 (P < 0.001) and triglycerides increased from 1.3+/-0.1 to 1.9+/-0.2 mmol/l at 6 months of treatment (P < 0.001). Serum low-density lipoprotein cholesterol levels remained unchanged during both treatments. Milder but similar changes in the subgroups of obese and non-obese women were observed during both treatments. Moreover, in the whole-study population both systolic (P = 0.02) and diastolic (P = 0.05) blood pressures decreased over the 6 months of metformin treatment. CONCLUSION: In women with PCOS, metformin treatment had beneficial effects on lipid profile and blood pressure, and therefore it could be useful in the prevention of cardiovascular complications in these women.

Adult↗
PubMed2006

Large maternal weight loss from obesity surgery prevents transmission of obesity to children who were followed for 2 to 18 years.

OBJECTIVE: Our aim was to compare the prevalence of obesity in 172 children who were aged 2 to 18 years and born to 113 obese mothers (BMI: 31 +/- 9 kg/m2) with substantial weight loss after biliopancreatic bypass surgery with 45 same-age siblings who were born before maternal surgery (mothers' BMI: 48 +/- 8 kg/m2) and with current population standards. METHODS: In this case series, with >88% follow-up in a tertiary referral center, cross sectional office chart and telephone data on childhood and adolescent weights were transformed to z scores. RESULTS: After maternal surgery, the prevalence of obesity in the offspring decreased by 52% and severe obesity by 45.1%, with no increase in the prevalence of underweight. The z score reduction in obesity was gender specific, with boys reducing from 1.4 +/- 1.3 before to 0.57 +/- 1.7 after maternal surgery, corrected for birth order. The difference was not significant in girls (0.8 +/- 1.3 vs 0.8 +/- 1.2). Among children of both genders who were aged 6 to 18 years of age and born after maternal surgery, the prevalence of overweight was reduced to population levels. CONCLUSIONS: Contrary to outcomes after intrauterine under- and overnutrition, the prevalence of overweight and obesity in children of mothers with large voluntary postsurgical weight loss was similar to that in the general population, with no increase in underweight. The results demonstrate the importance of potentially modifiable epigenetic factors in the cause of obesity.

Adolescent↗