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PubMed1996

Effects of ingested fructose and infused glucagon on endogenous glucose production in obese NIDDM patients, obese non-diabetic subjects, and healthy subjects.

Increased endogenous glucose production (EGP) and gluconeogenesis contribute to the pathogenesis of hyperglycaemia in non-insulin-dependent diabetes mellitus (NIDDM). In healthy subjects, however, EGP remains constant during administration of gluconeogenic precursors. This study was performed in order to determine whether administration of fructose increases EGP in obese NIDDM patients and obese non-diabetic subjects. Eight young healthy lean subjects, eight middle-aged obese NIDDM patients and seven middle-aged obese non-diabetic subjects were studied during hourly ingestion of 13C fructose (0.3 g.kg fat free mass-1.h-1) for 3 h. Fructose failed to increase EGP (measured with 6,6 2H glucose) in NIDDM (17.7 +/- 1.9 mumol.kg fat free mass-1.min-1 basal vs 15.9 +/- 0.9 after fructose), in obese non-diabetic subjects (12.1 +/- 0.5 basal vs 13.1 +/- 0.5 after fructose) and in lean healthy subjects (13.3 +/- 0.5 basal vs 13.8 +/- 0.6 after fructose) although 13C glucose synthesis contributed 73.2% of EGP in lean subjects, 62.6% in obese non-diabetic subjects, and 52.8% in obese NIDDM patients. Since glucagon may play an important role in the development of hyperglycaemia in NIDDM, healthy subjects were also studied during 13C fructose ingestion + hyperglucagonaemia (232 +/- 9 ng/l) and during hyperglucagonaemia alone. EGP increased by 19.8% with ingestion of fructose + glucagon (p < 0.05) but remained unchanged during administration of fructose or glucagon alone. The plasma 13C glucose enrichment was identical after fructose ingestion both with and without glucagon, indicating that the contribution of fructose gluconeogenesis to the glucose 6-phosphate pool was identical in these two conditions. We concluded that during fructose administration: 1) gluconeogenesis is increased, but EGP remains constant in NIDDM, obese non-diabetic, and lean individuals; 2) in lean individuals, both an increased glucagonaemia and an enhanced supply of gluconeogenic precursors are required to increase EGP; this increase in EGP occurs without changes in the relative proportion of glucose 6-phosphate production from fructose and from other sources (i.e. glycogenolysis + gluconeogenesis from non-fructose precursors).

Administration, Oral↗
PubMed1980

Anaerobic power output of young obese men: comparison with non-obese men and the role of excess fat.

Anaerobic power output was measured by the staircase climb test in 14 obese, 16 lean, and 21 ordinary men aged from 18--22 years. Fat storage rate (%fat) was estimated by densitometry. The obese group ranked highest with an average power output of 1,012 W. This value was significantly higher than those of the other two groups, 890 W for lean subjects and 855 W for ordinary subjects. The power output per kilogram of lean body mass of the obese group was the highest also. However, the vertical velocity was the lowest although the difference among the three average values was not statistically significant. To investigate the effect of excess fat, eight non-obese subjects engaged in an added-weight experiment. The value obtained was almost the same as for the obese group. The added weights made the vertical velocity decrease but the power output increase. Consequently, it was obvious that the excess fat of an obese man played a role only as an inert mass in the power output measurement. A significantly higher power output of the obese group might be due to more excess fat, and obesity itself was an advantage in the staircase climb test.

Adipose Tissue↗
PubMed2005

Increased expression of inflammation-related genes in cultured preadipocytes/stromal vascular cells from obese compared with non-obese Pima Indians.

AIMS/HYPOTHESIS: The specific contributions made by the various cell types in adipose tissue to obesity, particularly obesity-related inflammation, need to be clarified. The aim of this study was to elucidate the potential role of adipocyte precursor cells (preadipocytes/stromal vascular cells [SVC]). METHODS: We performed Affymetrix oligonucleotide microarray expression profiling of cultured abdominal subcutaneous preadipocytes/SVC isolated from the adipose tissue of 14 non-obese (BMI 25+/-4 kg/m2) and 14 obese (55+/-8 kg/m2) non-diabetic Pima Indian subjects. Quantitative real-time PCR (RT-PCR) was used to verify the differential expression of several genes in an independent group of subjects. RESULTS: We identified 218 differentially expressed genes with p values less than 0.01. Microarray expression profiling revealed that the expression of inflammation-related genes was significantly upregulated in preadipocytes/SVC of obese individuals. Quantitative RT-PCR confirmed the upregulation of IL8, CTSS, ITGB2, HLA-DRA, CD53, PLA2G7 and MMP9 in preadipocytes/SVC of obese subjects. CONCLUSIONS/INTERPRETATION: The upregulation of inflammation-related genes in preadipocytes/SVC of obese subjects may increase the recruitment of immune cells into adipose tissue and may also result in changes in the extracellular matrix (tissue remodelling) to accommodate adipose tissue expansion in obesity.

Adipocytes↗
PubMed2002

Polymorphisms in candidate obesity genes and their interaction with dietary intake of n-6 polyunsaturated fatty acids affect obesity risk in a sub-sample of the EPIC-Heidelberg cohort.

BACKGROUND/AIM: In several genes coding for molecules involved in the regulation of body weight (fat mass) and thermogenesis, polymorphisms have been reported which possibly modify human obesity risk. The aim of this study was a) to reproduce these observations with data and biological material from the Heidelberg cohort of EPIC, a large European prospective investigation into diet and cancer, and b) to investigate potential effects of interactions between dietary fatty acid intake and allelic variants on obesity risk. SUBJECTS AND METHODS: Within EPIC-Heidelberg, 154 subjects with a body mass index > 35 kg/m(2) and 154 age- and sex-matched normal-weight controls were selected and genotypes determined for 11 candidate genes. Dietary intake was assessed by a validated food frequency questionnaire. Odds ratios (OR) were computed by means of unconditional logistic regression and different adjustment models. Genotyping was performed by PCR-RFLP and allele-specific PCR. RESULTS: For most of the investigated genes (PPARA, PPARG2, UCP1, UCP2, UCP3, BAR-2, APM1, leptin, SORBS1, HSL, and TNFA) an indication for a minor effect on obesity risk was found. Indication of a risk-increasing effect was strongest for the homozygous form of leptin -2548AA with an adjusted OR of 3.53 (p < 0.009). Additionally, for the polymorphic sites of BAR-2 (Arg16Gly and Gln27Glu) a significant effect on obesity risk was seen. Importantly, the results of the analysis of gene-diet interactions suggest that the allelic variants of candidate genes (leptin, TNFA, PPARG2) might strongly affect diet-related obesity risk. CONCLUSIONS: The results support some but not all previous reports about a risk-modulating effect of polymorphisms in genes affecting obesity risk. The most important finding is an indication of substantial interaction between allelic variants of particular genes and fatty acid intake-related obesity risk. These observations suggest that future studies on polymorphisms in obesity genes should take data on dietary habits into account.

Adult↗
PubMed1992

Cardiomyopathy of obesity: a clinicopathologic evaluation of 43 obese patients with heart failure.

Right heart hemodynamic and endomyocardial biopsy abnormalities associated with marked obesity were characterized in 43 obese patients who presented with symptoms of congestive heart failure. Marked obesity was defined as a body mass index greater than or equal to 35 kg/m2. They were compared to a group of 409 patients with similar presentations but normal body mass. Analysis of the 519 patients showed that body mass index was positively correlated with right heart pressures and cardiac output (p less than or equal to 0.0001), pulmonary vascular resistance index (p less than or equal to 0.003) and systolic blood pressure (p less than or equal to 0.0006). Obese patients had elevated right heart pressures, cardiac output (p less than or equal to 0.0001) and pulmonary vascular resistance index (p less than or equal to 0.02) when compared with a group of lean patients with a similar degree of cardiomyopathy. After evaluation, a significantly higher percentage of obese patients were found to have idiopathic dilated cardiomyopathy compared with lean patients. A specific etiology was found in 264 (64.5%) of the 409 lean patients compared with 10 (23.3%) of the obese patients (p less than or equal to 0.0001). The most common finding on endomyocardial biopsy in the obese group was mild myocyte hypertrophy (67%). These data suggest that the cardiomyopathy of obesity exists and may play an important role in a population referred for the evaluation of heart failure.

Adult↗
PubMed1978

Pregnancy in the massively obese: course, outcome, and obesity prognosis of the infant.

The obstetric performance and pregnancy outcome in 208 massively obese patients who were delivered over an eight-year period were compared with those of nonobese control subjects. The incidence of obesity in their infants was also compared. No significant increase in the incidence of urinary tract infection, diabetes, breech presentation, cesarean section, forceps delivery, or maternal and infant morbidity was noted in the obese women. Significantly increased incidences of hypertensive disorders of pregnancy (p less than 0.01), gestational diabetes (p less than 0.01), inadequate weight gain (p less than 0.001), and wound or episiotomy infection (p less than 0.05) were observed in the study group. The mean birth weight of the infants of obese women was 209 grams greater than that of the control subjects. A significantly increased number of the obese patients were delivered of excessive-sized infants. Despite this, the incidence of obesity in infants of obese women was not significantly increased at birth or six months of age. By 12 months of age, however, these infants were significantly more obese than the control infants.

Adolescent↗
PubMed1987

Glucagon and insulin response to meals in non-obese and obese Dutch women.

Many digestive complaints are associated with abnormalities in gastrointestinal peptide hormone function. To investigate the effect of obesity on the release of pancreatic peptide hormones, we have compared the release of insulin and glucagon in non-obese-obese Dutch women in response to isocaloric mixed meals and to Naloxone, an opioid antagonist. Healthy premenopausal women who were separated into three groups based on body mass index (BMI less than 23; 23-27, greater than 28), were fed 600-calorie breakfasts. Higher fasting levels of plasma insulin and glucagon occurred in obese (BMI greater than 28) than lean (BMI less than 23) women, while glucagon and insulin release after a high fat meal occurred in obese women. Naloxone administration in obese women decreased plasma insulin and glucagon, but in lean women, naloxone increased plasma glucagon but did not alter plasma insulin levels. Results indicate differences in opiate effects on pancreatic function in non-obese-obese women.

Adult↗
PubMed1989

Obesity as a risk factor in drug-induced organ injury. III. Increased liver and kidney injury by furosemide in the obese overfed rat.

Effects of the diuretic drug furosemide were examined in obese animals to evaluate the hypothesis that organ damage by reactive drug metabolites may be potentiated by this disease. Obese overfed Sprague-Dawley rats that were treated ip with 450 mg/kg furosemide on the basis of total body mass suffered a 58% mortality rate over 24 h. This contrasted with 0% mortality in animals of normal body mass. On the basis of median histopathology scores, organ necrosis was judged to be greater in the liver (2+) and kidneys (1+) of obese rats than in the liver (1+) and kidneys (less than 1+) of normal controls (p less than 0.05). Obese animals demonstrated a fourfold rise in fat mass over controls. The low solubility of furosemide in lipid makes it probable that aggravated drug toxicity in obese rats dosed to total body mass resulted in part from elevated furosemide concentrations in lean body mass. In a subsequent study designed to minimize this possibility, furosemide was administered on the basis of fat-free body mass to equalize initial drug exposure in obese and control rats. Even with this downward dosage adjustment, obese animals suffered increased hepatic necrosis (median score of 2+ versus 0 in treated controls), greater impairment of renal function (plasma creatinine concentration of 2.41 mg/dl versus 0.96 mg/dl in treated controls), and more extensive enzymuria (enzyme excretion 175-300% more elevated than in treated controls). In conclusion, obese rats appear to be at increased risk of furosemide-induced liver and kidney injury due to at least two factors: (1) increased exposure of target organs in lean body mass to furosemide when the dosing of this poorly lipophilic drug was based on total body mass, and (2) increased susceptibility of target organs in lean body mass to furosemide injury when dosing was adjusted downward to reflect fat-free body mass and to equalize initial drug exposure.

Animals↗
PubMed1999

Intracellular hyperinsulinism: a metabolic characteristic of obesity with and without Type 2 diabetes: intracellular insulin in obesity and Type 2 diabetes.

There is evidence that intracellular insulin may carry out some insulin mediated actions, including glucose transport. As intracellular insulin has never been quantitatively assessed in human cells, we evaluated its concentrations in monocytes from normal subjects (n = 7) and obese patients without (n = 9) and with Type 2 diabetes mellitus (n = 10). After the incubation of cells with labeled insulin for 60 min at 37 degrees C, intracellular intact insulin concentrations were measured by HPLC and expressed as pmol x 10(-6). Insulin concentrations were higher (ANOVA P < 0.01) within cells from obese (115.4 +/- 26.4 pmol x 10(-6)/2 x 10(5) cells) and obese diabetic patients (93.2 +/- 36.3 pmol x 10(-6)/2 x 10(5) cells) compared with normal cells (28.5 +/- 13.1 pmol x 10(-6)/2 x 10(5) cells). Moreover, after insulin was removed from the incubation medium the decrease of intracellular insulin was significantly lower (P < 0.01) in cells from both obese and obese diabetic patients than in normal subjects. Intracellular undissociated insulin-insulin receptor complexes on average, increased 2-fold (P < 0.01) in cells from insulin resistant patients compared with normal cells. Finally, in downregulated cells from obese and obese diabetic patients, the recycling of the internalized insulin receptor was completely disrupted. In conclusion, monocytes from obese patients with and without Type 2 diabetes mellitus, present increased intracellular insulin concentrations and these conditions are associated with a significant impairment of insulin receptor processing. Increased intracellular insulin concentration in cells from these patients may be necessary in order to overcome insulin resistance.

Chromatography, High Pressure Liquid↗
PubMed2000

Leptin concentration in non-obese and obese children with type 1 diabetes mellitus.

Leptin, the product of the ob gene, is an adipocyte-derived hormone that positively correlates with body fat percantage and body mass index (BMI). There are many data which demonstrate a significant relationship between leptin and insulin, but the mechanism underlying the changes of leptin induced by insulin and vice versa remains to be studied in more detail. In this review, we analysed the data on the behaviour of serum leptin levels in non-obese and obese children with type 1 diabetes mellitus. It has been shown that the diminished serum leptin concentrations in patients with newly discovered insulin-dependent diabetes mellitus (IDDM) could be caused by insulin deficiency and/or increased lipolysis. Moreover, while in some studies in diabetic children with good metabolic control the serum leptin levels are similar to those of healthy children, in other studies children with IDDM have leptin levels higher than non diabetic children; it is possible that in some diabetic children intensified insulin therapy could cause chronic hyperinsulinemia with high leptin levels. The mean serum leptin concentrations in the obese diabetic subjects were significantly higher when compared with non-obese diabetics. Obese diabetic patients showed no significant differences in leptin concentrations in comparison to the non diabetic obese group matched by age, sex and BMI. In obese diabetics, during weight loss, independent of the quality of metabolic control, serum leptin concentration declines. The changes of leptin in diabetes seem to be similar to those observed in healthy obese subjects.

Adult↗
PubMed2004

Obesity and awareness of obesity as risk factors for breast cancer in six ethnic groups.

OBJECTIVE: To document BMI and knowledge regarding obesity as a risk factor for breast cancer among subpopulations of African-, Caribbean-, and European-American women and to consider the variables predicting obesity in these diverse groups. RESEARCH METHODS AND PROCEDURES: A stratified cluster-sampling plan was used to recruit 1364 older women from Brooklyn, NY, during 2000-2002. Two groups were born in the United States (African Americans and European Americans), whereas others were from the English-speaking Caribbean, Haiti, the Dominican Republic, and Eastern Europe. Participants provided demographics, height and weight measures, and estimates of the risk obesity posed for breast cancer. RESULTS: Women from all groups were significantly overweight (BMI > 25 kg/m(2)), although European Americans were lowest, followed by Dominicans and Haitians; African-American and English-speaking Caribbean women fell into the obese range, even when background variables were controlled. Knowledge of obesity as a breast cancer risk factor was also poor across groups, but Dominicans and Haitians had the lowest scores on knowledge. Importantly, knowledge was not associated with BMI in the overall sample, even when controlling for demographics and ethnicity, although logistic regressions comparing normal weight women with overweight and obese groupings suggested some knowledge of breast cancer risk in the overweight, but not the obese, group. DISCUSSION: The findings remind health professionals of the need to consider more specific ethnic groupings than has hitherto been the case, as well as consider how ethnic and cultural variables may influence perceptions of obesity and its relation to cancer risk.

Black or African American↗
PubMed2005

Geographic variation in the prevalence of obesity, diabetes, and obesity-related behaviors.

OBJECTIVE: To examine the variation in the prevalences of obesity and type 2 diabetes in weight loss counseling by health providers and in other potential obesity-related determinants in 100 metropolitan statistical areas in the United States. RESEARCH METHODS AND PROCEDURES: We performed a cross-sectional study using data from the 2000 Behavioral Risk Factor Surveillance System, the largest telephone survey of health behaviors in the United States, of age-adjusted prevalence of obesity, type 2 diabetes, intake of >or=five servings of fruits and vegetables per day, participation in 150 minutes of leisure-time physical activity per week, receipt of weight management advice, and reports of trying to lose or maintain weight among men and women more than 18 years old. RESULTS: The age-adjusted prevalence of obesity ranged from 13.1% to 30.0% and that of type 2 diabetes from 3.3% to 9.2%. Among participants who had visited a physician for a routine checkup in the previous 12 months, 13.1% to 27.1% of all participants recalled receiving advice from a health professional about their weight, and 11.7% to 34.6% of overweight or obese participants recalled receiving advice to maintain or lose weight. DISCUSSION: Significant differences in the prevalence of obesity and self-reported type 2 diabetes and in medical practice patterns regarding weight management advice exist among metropolitan statistical areas. These results suggest important opportunities to investigate reasons for these variations that could potentially be used to mitigate the current epidemic of obesity and to identify areas where obesity and diabetes prevention efforts may need to be targeted.

Adult↗
PubMed2006

Chronic dietary vitamin A supplementation regulates obesity in an obese mutant WNIN/Ob rat model.

OBJECTIVE: To understand the possible role of chronic dietary high vitamin A supplementation in body weight regulation and obesity using a novel WNIN/Ob obese rat model developed at the National Centre for Laboratory Animal Sciences of National Institute of Nutrition, India. RESEARCH METHODS AND PROCEDURES: Thirty-six 7-month-old male rats of lean, carrier, and obese phenotypes were broadly divided into two groups; each group was subdivided into three subgroups consisting of six lean, six carrier, and six obese rats and received diets containing either 2.6 or 129 mg vitamin A/kg of diet for 2 months. Body weight gain, food intake, and weights of various organs were recorded. Adiposity index and BMI were calculated. Serum and liver retinol and brown adipose tissue (BAT)-uncoupling protein1 (UCP1) mRNA expression levels were quantified. RESULTS: Chronic feeding of high but non-toxic doses of vitamin A through diet significantly reduced (P < or = 0.05) body weight gain, adiposity index, and retroperitoneal white adipose tissue mass (without affecting food intake) in obese rats compared with their lean and carrier counterparts. In general, vitamin A treatment significantly improved hepatic retinol stores (P < or = 0.05) in all phenotypes without affecting serum free retinol levels. However, augmented BAT-UCP1 expression was observed only in carrier and obese rats (whose basal expression was low). DISCUSSION: Our data suggest that chronic dietary vitamin A supplementation at high doses effectively regulates obesity in obese phenotype of the WNIN/Ob strain, possibly through up-regulation of the BAT-UCP1 gene and associated adipose tissue loss. However, in vitamin A-supplemented lean and carrier rats, changes in adiposity could not be related to BAT-UCP1 expression levels.

Adipose Tissue↗
PubMed1994

Plasma adrenaline concentration is lower in post-obese than in never-obese women in the basal state, in response to sham-feeding and after food intake.

1. Plasma pancreatic polypeptide, plasma catecholamine, blood glucose, plasma insulin and plasma peptide YY concentrations were studied to assess differences between eight formerly obese and eight never-obese control women during 25 min of sham-feeding (with the sight and smell of an English breakfast) and for 5 h after they had ingested the meal (3514 kJ, 50% fat, 35% carbohydrate). The post-obese women had maintained their normal body weight for at least 3 months before the study. 2. The plasma noradrenaline concentration was not different between the groups either during fasting (post-obese women 0.08 +/- 0.01 ng/ml versus control women 0.10 +/- 0.01 ng/ml) or in the significant postprandial increase (P < 0.001). The plasma adrenaline concentration increased significantly during sham-feeding in the control group from 0.024 +/- 0.004 ng/ml to 0.033 +/- 0.004 ng/ml (P = 0.02) in contrast with the post-obese women, who had significantly lower plasma concentrations of adrenaline in the fasting state (post-obese 0.016 +/- 0.003 ng/ml versus control women 0.024 +/- 0.004 ng/ml, P = 0.003), during sham-feeding (post-obese women 0.018 +/- 0.002 ng/ml versus control women 0.033 +/- 0.004 ng/ml, P = 0.003) and in the postprandial increase (P = 0.003). The maximal postprandial response concentrations recorded 5 h after the meal were 0.025 +/- 0.003 ng/ml in post-obese women and 0.035 +/- 0.004 ng/ml in control subjects (P = 0.04). There were no significant differences in plasma pancreatic polypeptide, plasma peptide YY, plasma insulin, or blood glucose concentrations between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2005

The aerobic fitness (VO2 peak) and alpha-fibrinogen genetic polymorphism in obese and non-obese Chinese boys.

The purpose of the study was to compare the aerobic fitness (VO (2) peak) between obese and non-obese boys at pre-puberty and examine the effect of body composition on VO (2) peak in this cohort with reference to TaqI polymorphism at alpha-fibrinogen gene locus. Seventy-seven Chinese boys with similar lifestyle participated in the study. Among them, 47 were diagnosed as obese. VO (2) peak was measured by a treadmill test and body composition was assessed via a combined anthropometrical and bioelectrical impedance analysis method. The alpha-fibrinogen genetic polymorphism was detected through PCR-based digestion with TaqI restriction enzyme. The results indicated that VO (2) peak was significantly lower in obese boys compared with normal weight counterparts when the data were expressed either in conventional ratio unit (ml (-1) . min (-1) . lean body weight [LBW] (-1)) or in allometric unit (ml (-1) . min (-1) . body weight [BW] (-2/3)). LBW, fat mass (FM), and body fat content (BF %) all were correlated with VO (2) peak, while LBW was the strongest predictor. The relationship between body composition and VO (2) peak seemed quite comparable across different alpha-fibrinogen genotypes. Significant difference was observed between obese and non-obese boys in terms of the proportion of genotypes and frequency of alleles. T1T1 homozygotes had higher risk for obesity. We came to the conclusion that prepubertal obese boys exhibited impaired aerobic fitness compared with their normal weight peers. VO (2) peak is closely related to LBW and independent of FM. This relationship remains constant irrespective of the TaqI alpha-fibrinogen genotypes that may be associated with fatness in boys.

Body Composition↗
PubMed2007

Circulating serum adiponectin concentrations do not differ between obese and non-obese caucasians and are unrelated to insulin sensitivity.

Reduced serum levels of adiponectin in obesity and insulin resistance seem paradoxical, since adipose tissue is the only source of adiponectin, and reports on that subject are contradictory. The aim of this study was to investigate the concentrations of adiponectin in non-obese and obese normoglycemic humans, and to determine the correlation between adiponectin and HOMA index of insulin sensitivity. Based on the WHO definition of obesity, 145 obese subjects and 49 non-obese controls (aged 20-55 years) were studied. The serum adiponectin concentrations did not differ between subjects and controls (p=0.6398) and were not correlated with HOMA index (r=-0.0211; p=0.8048, and r=-0.0523; p=0.4757, for subjects and controls, respectively). Adiponectin was not correlated with HOMA index in females (r=-0.0521; p=0.6546, and r=-0.0825; p=0.3981, for female subjects and controls, respectively) as well as in males (r=0.0033; p=0.9791, and r=0.0123; p=0.9131, for male subjects and controls, respectively). These results lead to the conclusion that neither the concentrations of adiponectin differ between obese and non-obese humans, nor does any relationship between adiponectin concentration and insulin sensitivity exist.

Adiponectin↗
PubMed1994

Locus of control orientation among obese adults in outpatient treatment for obesity.

We studied locus of control (LOC) in samples of obese and nonobese subjects. We administered Rotter's (1966) I-E Scale to 106 obese adults in outpatient treatment for obesity and to 99 nonobese controls. The obese subjects were significantly more internally oriented than the control group. These findings challenge currently held assumptions on the directionality of LOC in obese groups. The results contradict the consensus among researchers that obese individuals have an external LOC orientation. The finding that internal LOC is associated with the obese condition may be a useful predictor variable influencing obesity treatment, approaches, and outcome.

Adult↗
PubMed1989

Fatness and obesity of the parents of obese individuals.

As shown in 1419 pairings of obese probands with their parents drawn from a larger series of greater than 9000 proband-parent pairings, the fathers and mothers of obese probands are of increased fatness level (+0.27 Z scores) and more often obese than expected (odds ratio 1.50 overall). However, the tendency towards increased fatness and a greater prevalence of obesity among the parents of obese probands bears a curvilinear relationship to the age of the proband, being least when the probands are young, peaking when the sons and daughters are teen-agers, and declining thereafter. Parents of lean probands in turn tend to be lean themselves (averaging -0.25 Z scores) and least often obese when their progeny are teen-aged. As shown in a two-generational context, familial obesity is best demonstrated in adolescents and their parents, either reflecting years spent in common or a specific etiology for adolescent-onset obesity.

Adolescent↗