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At least 487 records · Page 27Linked to original sources
PubMed2001

Blood pressure and pulse pressure during long-term weight loss in the obese: the Swedish Obese Subjects (SOS) Intervention Study.

OBJECTIVE: Recently we reported a complete relapse in the blood pressure (BP) of obese subjects despite a maintained 16% weight loss over 8 years. This relapse is now analyzed as a function of several variables. Pulse pressure (PP) is an independent risk factor of cardiovascular mortality. We now examine the development of PP in the obese and whether it can be modified by weight-reducing gastric surgery. RESEARCH METHODS AND PROCEDURES: A total of 1157 patients treated with gastric surgery and 1031 obese controls (body mass index of 41.0 +/- 4.6 kg/m(2) [mean +/- SD], age 48 +/- 6 years) were followed for 5.5 +/- 2.1 (range 3 to 10) years. To separate the effect of weight change from effect of time on BP, the patients were divided in cohorts based on follow-up time. RESULTS: Gastric surgery resulted in a maximum weight loss after 1 year that was followed by a moderate relapse. After 5.5 years, weight loss in the intervention group was 18 +/- 11% of initial body weight. Very little weight change was seen in controls. Systolic BP decreased in the intervention group during the first 6 months but had relapsed to control values at last examination. The adjusted change in PP was +4.7 mm Hg in obese controls but +2.9 mm Hg in the intervention group (p < 0.001). Final BP values were more closely related to follow-up time and ongoing weight increase than to initial body weight or initial weight loss. DISCUSSION: Effects of time (aging) and weight change per year on BP can be separated. An early increase in PP could be observed in the obese. This increase could be modified by weight-reducing gastric surgery.

Adult↗
PubMed2002

The obesity epidemic: pathophysiology and consequences of obesity.

Obesity has reached epidemic proportions in the United States: more than 20% of adults are clinically obese as defined by a body mass index of 30 kg/m(2) or higher, and an additional 30% are overweight. Environmental, behavioral, and genetic factors have been shown to contribute to the development of obesity. Elevated body mass index, particularly caused by abdominal or upper-body obesity, has been associated with a number of diseases and metabolic abnormalities, many of which have high morbidity and mortality. These include hyperinsulinemia, insulin resistance, type 2 diabetes, hypertension, dyslipidemia, coronary heart disease, gallbladder disease, and certain malignancies. This underscores the importance of identifying people at risk for obesity and its related disease states.

Adipose Tissue↗
PubMed2005

Increased cortisol bioavailability, abdominal obesity, and the metabolic syndrome in obese women.

OBJECTIVE: This study was conducted to obtain a detailed profile of hypothalamo-pituitary-adrenal (HPA) axis activity and reactivity and its differential relationships with body fat distribution and total fat mass in premenopausal obese women. RESEARCH METHODS AND PROCEDURES: Cortisol responses to stimulation (awakening, food intake, exercise) and suppression (0.25 mg dexamethasone), cortisol metabolism, and tissue sensitivity to glucocorticoids were studied in 53 premenopausal obese women grouped according to their waist-to hip ratio: women with abdominal body fat distribution (A-BFD; n = 31) and women with peripheral fat distribution (P-BFD; n = 22). RESULTS: Comparatively, A-BFD women had 1) lower awakening salivary cortisol levels; 2) increased salivary responsiveness to a standardized lunch; 3) similar pituitary sensitivity to dexamethasone but decreased sensitivity of monocytes to dexamethasone; 4) similar 24-hour urinary free cortisol but increased 24-hour urinary ratio of cortisone-to-cortisol; and 5) no difference in corticosteroid binding protein parameters. DISCUSSION: Although abdominal obesity is not very different from generalized obesity in terms of HPA function, subtle variations in HPA axis activity and reactivity are evidenced in A-BFD premenopausal obese women.

Abdomen↗
PubMed1998

What is "obesity"--an analysis of referral letters to an obesity unit.

OBJECTIVES: To evaluate the quality of referral letters concerning obese patients from general practice and other specialities to an obesity unit. DESIGN: Retrospective analysis of referral letters in 500 consecutive patient records. SETTING: Academic specialist obesity unit. RESULTS: Most letters came from general practice (70%), followed by internal medicine/endocrinology (12%). Information on body weight was missing in 13% of all referrals and on height in 24%. Waist circumference was mentioned in 1%. Relevant data substantiating possible comorbidities, in particular the metabolic syndrome, was missing in 92-97%. Relevant medication was indicated in 22% of the referrals. On a 3-point, graded global evaluation scale of the referral quality, only 7% of all letters were found to be 'ideal'. CONCLUSION: The low professional quality of these referrals may reflect the fact that physicians find the term 'obesity' enough to warrant the referral without further specifications. An alternative explanation for the inadequate referrals is the well documented negative attitude of physicians, who consider obesity as sloth and as a self-inflicted condition, not necessitating further medical details.

Adult↗
PubMed2001

Parental influences on laboratory eating behavior in obese and non-obese children.

OBJECTIVE: To determine parental influence on obesity, eating behavior of 80 obese and normal weight children (aged 8-12 y) was investigated in the laboratory. DESIGN: A controlled repeated measurement design was used. The mother was either present or absent while the child was eating in the laboratory. MEASUREMENTS: The eating style was measured by recording cumulative eating curves with a universal eating monitor, using yoghurt as a standardized experimental meal. RESULTS: The eating behavior of obese children differed significantly from normal weight children only when the mother was present in the laboratory. Overweight children ate faster with larger bites and showed an acceleration of their eating rate towards the end of the meal. CONCLUSION: Such an eating style can be hypothesized to explain an increased calorie intake in obese children, promoting a positive energy balance in the long-term. The data support a learning model of obesity in childhood, which also has implications for family treatment.

Child↗
PubMed2002

Blood pressure in relation to relative weight at birth through childhood and youth in obese and non-obese adult men.

OBJECTIVE: To determine the influence on blood pressure of relative weight from birth through adulthood in non-obese and juvenile obese men. DESIGN: Case-cohort study of obesity in Danish men, identified at age (mean+/-s.d.) 19.8+/-1.6 y at draft board examination, who participated in at least one of two follow-up studies in adulthood (age 36.8+/-6.7 and 47.9+/-6.8 y at first and second follow-up, respectively). Birth weight and weight and height from the age of 7-13 y were collected from school health records. SUBJECTS: Three hundred and twenty-seven non-obese men (controls) selected as 0.5% of the draft board population and 285 obese men with body mass index (BMI)> or =31 kg/m(2) at draft board examination. MAIN OUTCOME MEASURES: Systolic and diastolic blood pressure measured twice in adulthood adjusted for current age. RESULTS: Birth weight was inversely related to systolic blood pressure at first and second follow-up, but only significantly so when adjusted for current BMI (regression coefficients in mmHg per unit Z-score (95% confidence interval (CI))-1.2 (-2.3, -0.1) and -1.6 (-3.1, 0.0)). Change in Z-score from birth weight to BMI at the age of 7 y was significantly positively related to systolic blood pressure, but the relationship weakened by adjustment for current BMI (0.8 (0.1, 1.6) and 0.6 (-0.4, 1.6), respectively). If both birth weight and change until 7 y were included in the same model, their effects were both positive and significant, but they weakened and became not significant when adjusted for current BMI. BMI since the age of 7 y had no significant effect on blood pressure beyond that of current BMI. CONCLUSION: In a wide range of adult BMI in men, the birth weight was inversely related to systolic blood pressure, even when controlled for BMI since the age of 7 y. However, the effect may reflect the weight change between birth and 7 y of age. After that age BMI had no additional effect on blood pressure beyond the effect of current BMI.

Adolescent↗
PubMed2005

Weight history from birth through childhood and youth in relation to adult lung function, in Danish juvenile obese and non-obese men.

OBJECTIVE: To investigate the associations of birth weight, body mass index (BMI) during childhood and youth, and current BMI with adult lung function. DESIGN: Population-based longitudinal study of juvenile obese and non-obese men, who were identified at draft board examination (age range: 19-27 y) and who participated in a follow-up examination in 1981-1983 (age range: 25-48 y). Birth weight, childhood weight and height measurements from 7 to 13 y of age were obtained from school health records. Current BMI and lung function were assessed at follow-up. SETTING: Copenhagen and adjacent regions, Denmark. SUBJECTS: In total, 193 juvenile obese men at draft board examination and 205 randomly selected nonobese controls from the same population. MAIN OUTCOME MEASURES: Lung function measured by forced expiratory volume in 1 s (FEV(1)) and forced vital capacity (FVC), adjusted for age and height. RESULTS: After adjusting for current BMI, smoking and education, birth weight was positively related to FEV(1), although only with borderline statistical significance. BMI at age 7 y was positively associated with both FEV(1) and FVC, whereas BMI at later ages in childhood and in youth was not associated with these measures. There was a strong negative linear relation between current BMI and lung function among those currently overweight and obese (BMI 25 kg/m(2)), whereas no association was seen in the non-obese (BMI <25 kg/m(2)). CONCLUSION: Our findings confirm the detrimental effect of high current BMI on adult lung function, and further suggest that early childhood growth has a protective influence.

Adolescent↗
PubMed2006

A new approach to assessing the health benefit from obesity interventions in children and adolescents: the assessing cost-effectiveness in obesity project.

OBJECTIVE: To report on a new modelling approach developed for the assessing cost-effectiveness in obesity (ACE-Obesity) project and the likely population health benefit and strength of evidence for 13 potential obesity prevention interventions in children and adolescents in Australia. METHODS: We used the best available evidence, including evidence from non-traditional epidemiological study designs, to determine the health benefits as body mass index (BMI) units saved and disability-adjusted life years (DALYs) saved. We developed new methods to model the impact of behaviours on BMI post-intervention where this was not measured and the impacts on DALYs over the child's lifetime (on the assumption that changes in BMI were maintained into adulthood). A working group of stakeholders provided input into decisions on the selection of interventions, the assumptions for modelling and the strength of the evidence. RESULTS: The likely health benefit varied considerably, as did the strength of the evidence from which that health benefit was calculated. The greatest health benefit is likely to be achieved by the 'Reduction of TV advertising of high fat and/or high sugar foods and drinks to children', 'Laparoscopic adjustable gastric banding' and the 'multi-faceted school-based programme with an active physical education component' interventions. CONCLUSIONS: The use of consistent methods and common health outcome measures enables valid comparison of the potential impact of interventions, but comparisons must take into account the strength of the evidence used. Other considerations, including cost-effectiveness and acceptability to stakeholders, will be presented in future ACE-Obesity papers. Information gaps identified include the need for new and more effective initiatives for the prevention of overweight and obesity and for better evaluations of public health interventions.

Adolescent↗
PubMed2006

Common familial influences on clustering of metabolic syndrome traits with central obesity and insulin resistance: the Kiel obesity prevention study.

OBJECTIVE: The phenotypic heterogeneity of metabolic syndrome (MSX) suggests heterogeneity of the underlying genotype. The aim of the present study was to examine the common genetic background that contributes to the clustering between the two main features (insulin resistance, central obesity) and different MSX component traits. METHODS: In all, 492 individuals from 90 families were investigated in a three-generation family path study as part of the Kiel Obesity Prevention Study (KOPS, 162 grandparents, 66.1+/-6.7 years, 173 parents, 41.3+/-5.4 years and 157 children, 10.8+/-3.4 years). Overall heritability was estimated and common familial (genetic and environmental) influences on insulin resistance (HOMA-IR) or central obesity (elevated waist circumference, WC), respectively, and different MSX traits were compared in a bivariate cross-trait correlation model. RESULTS: Prevalence of MSX (according to NCEP criteria) was 27.2% (f) and 27.8% (m) in adults and 3.5% (f) and 8.5% (m) in children and adolescents, respectively. MSX phenotype was found to be highly variable, comprising 16 subtypes of component trait combinations. Within-trait heritability was 38.5% for HOMA-IR and 53.5% for WC, cross-trait heritability was 53.4%. As much as 6-18% and 3-10% of the shared variance between different MSX component traits (lipid profile, blood pressure) and WC or HOMA-IR, respectively, may be genetic. With the exception of HDL-C, the shared genetic variance between MSX component traits and WC was higher than the genetic variance shared with HOMA-IR. CONCLUSION: A common genetic background contributes to the clustering of different MSX component traits and central obesity or insulin resistance. Common genetic influences favour central obesity as a major characteristic linking these traits.

Adult↗
PubMed2003

Possible involvement of the adipose tissue renin-angiotensin system in the pathophysiology of obesity and obesity-related disorders.

Angiotensin II (Ang II), acting on the AT1 and AT2 receptors in mammalian cells, is the vasoactive component of the renin-angiotensin system (RAS). Several components of the RAS have been demonstrated in different tissues, including adipose tissue. Although the effects of Ang II on metabolism have not been studied widely, it is intriguing to assume that components of the RAS produced by adipocytes may play an autocrine, a paracrine and/or an endocrine role in the pathophysiology of obesity and provide a potential pathway through which obesity leads to hypertension and type 2 diabetes mellitus. In the first part of this review, we will describe the production of Ang II, the different receptors through which Ang II exerts its effects and summarize the concomitant intracellular signalling cascades. Thereafter, potential Ang II-induced mechanisms, which may be associated with obesity and obesity-related disorders, will be considered. Finally, we will focus on the different pharmaceutical agents that interfere with the RAS and highlight the possible implications of these drugs in the treatment of obesity-related disorders.

Adipose Tissue↗
PubMed2001

Metformin reduces weight, centripetal obesity, insulin, leptin, and low-density lipoprotein cholesterol in nondiabetic, morbidly obese subjects with body mass index greater than 30.

We studied 31 nondiabetic, habitually (> or =5 years) morbidly obese subjects (mean +/- SD body mass index [BMI] 43 +/- 8.7, median 43). Our specific aim was to determine whether metformin (2.55 g/d for 28 weeks) would ameliorate morbid obesity and reduce centripetal obesity; lipid and lipoprotein cholesterol, insulin, and leptin levels; and plasminogen activator inhibitor activity (PAI-Fx), risk factors for coronary heart disease (CHD). The patients were instructed to continue their prestudy dietary and exercise regimens without change. After 2 baseline visits 1 week apart, the 27 women and 4 men began receiving metformin, 2.55 g/d, which was continued for 28 weeks with follow-up visits at study weeks 5, 13, 21, and 29. Daily food intake was recorded by patients for 7 days before visits then reviewed with a dietitian. Kilocalories per day and per week were calculated. At each visit, fasting blood was obtained for measurement of lipid profile, insulin, leptin, and PAI-Fx. The mean +/- SD kilocalories consumed per day, 1,951 +/- 661 at entry, fell by week 29 to 1,719 +/- 493 (P =.014) but did not differ at weeks 5, 13, and 21 from that at week 29 (P >.2). Weight fell from 258 +/- 62 pounds at entry to 245 +/- 54 pounds at week 29 (P =.0001). Girth was reduced from 51.8 +/- 6.2 to 49.2 +/- 4.5 inches (P =.0001). Waist circumference fell from 44.0 +/- 6.4 inches to 41.3 +/- 5.9 (P =.0001). The waist/hip ratio fell from 0.85 +/- 0.09 to 0.84 +/- 0.09 (P =.04). Fasting serum insulin, 28 +/- 15 microU/mL at entry, fell to 21 +/- 11 microU/mL at week 29 (P =.0001), and leptin fell from 79 +/- 33 ng/mL to 55 +/- 27 ng/mL (P =.0001). On metformin, there were linear trends in decrements in weight, girth, waist circumference, waist/hip ratio, insulin, and leptin throughout the study period (P <.007). Low-density lipoprotein (LDL) cholesterol, 126 +/- 34 mg/dL at study entry, fell to 112 +/- 43 mg/dL at week 29 (P =.001), with a linear trend toward decreasing levels throughout (P =.036). By stepwise linear regression, the higher the entry weight, the larger the reduction in weight on metformin therapy (partial R(2) = 31%, P =.001). The greater the reduction in kilocalories consumed per day, the greater the decrease in weight on metformin therapy (partial R(2) = 15%, P =.011). The higher the waist/hip ratio at entry, the greater its reduction on metformin therapy (partial R(2) = 11%, P =.004). The higher the entry serum leptin, the greater its reduction on metformin therapy (partial R(2) = 29%, P =.002). The greater the reduction in insulin on metformin, the greater the reduction in leptin (partial R(2) = 8%, P =.03). The higher the entry PAI-Fx, the greater the reduction in PAI-Fx on metformin (partial R(2) = 43%, P =.0001). Metformin safely and effectively reduces CHD risk factors (weight, fasting insulin, leptin, LDL cholesterol, centripetal obesity) in morbidly obese, nondiabetic subjects with BMI > 30, probably by virtue of its insulin-sensitizing action.

Adult↗
PubMed2001

Study of the effect of changing glucose, insulin, and insulin-like growth factor-I levels on serum corticosteroid binding globulin in lean, obese, and obese subjects with glucose intolerance.

We have previously described that serum corticosteroid binding globulin (CBG) concentrations are associated with insulin secretion. The present study was designed to evaluate the effects of changing insulin concentrations, both endogenous and after exogenous insulin administration, on circulating CBG levels in vivo. Serum CBG concentrations were measured during an insulin-modified frequently sampled intravenous (IV) glucose tolerance test (FSIVGT) in 14 lean and 19 obese otherwise healthy subjects with varying degrees of glucose tolerance. Acute insulin response to glucose (AIRg) correlated significantly with serum CBG concentrations at time 0 (r = -.38, P =.029), 22 minutes (r = -.41, P =.01), 50 minutes (r = -.41, P =.01), and 180 minutes (r = -.39, P =.02). Insulin sensitivity (S(I)) was not associated with serum CBG concentration at time 0 (r = -.16, P = not significant [NS]), but correlated significantly with CBG concentration at 22 minutes (r = -.41, P =.02) and 50 minutes (r = -.35, P =.048) of the FSIVGT. In lean subjects, serum CBG concentration decreased significantly after IV insulin from 37.9 +/- 5.4 to 35.4 +/- 3 mg/L (P =.02) and returned to basal levels thereafter. In contrast, obese, glucose-tolerant subjects had lower CBG levels than lean and obese glucose intolerant subjects (33.8 +/- 3.0 v 37.9 +/- 5.4 and 39.8 +/- 4.4 mg/L, respectively), and their serum CBG concentrations remained unchanged during FSIVGT. Mean serum-free insulin-like growth factor-I (IGF-I) concentrations steadily declined from 1.21 +/- 0.81 to 0.8 +/- 0.36 microg/L during the FSIVGT, and this effect was restricted to lean subjects. Basal serum-free IGF-I did not correlate with CBG levels at time 0, but correlated inversely with the serum CBG concentrations at 22 minutes (r = -.36, P =.04). Stepwise multivariant analysis showed that AIRg (P =.035) and S(I) (P =.046), but not free IGF-I levels, independently contributed to 28% of CBG variance at 22 minutes. These results suggest that insulin, but not IGF-I, constitutes an important negative regulator of CBG liver synthesis. Endogenous and exogenous insulin do not affect serum CBG concentrations in insulin-resistant obese subjects with preserved or decreased insulin secretion. Obese glucose-tolerant subjects are hypothesized to exhibit tonically inhibited serum CBG levels. In contrast, in lean subjects, the higher the insulin secretion the lower the serum CBG concentration. The mechanisms of this CBG inhibitory effect exerted by insulin and its implication on cortisol homeostasis and fat distribution in humans await further investigations.

Adult↗
PubMedDate not supplied

Epidemiologic and metabolic risk factors for childhood obesity. Prepared for the Fourth Congress on Obesity Research, Vienna, Austria, December 1988.

The data reviewed here emphasize the suggestion that obesity in children is the result of an interaction between a susceptible host and an environment that promotes the disease. A variety of environmental factors are related to childhood obesity. Nonetheless, except for television viewing, the behavioral correlates of the environmental associations remain unspecified. The goal for the coming decade is the identification of these behaviors, and their modification. The last five years have witnessed a dramatic increase in our understanding of the components of energy expenditure, and their relationship to the development of obesity. Both the early studies of Griffith and Payne, and the more recent studies of infants by Roberts suggest that reduced energy spent on activity may be the constitutional feature that accounts for an increased susceptibility to the disease. Reduced energy spent on activity may also account for some of the epidemiologic correlates. For example, differences in activity may account for the regional, seasonal, and population density effects on obesity, as well as some of the family line variables such as parental obesity, and family size. All represent promising sources for future investigation.

Adolescent↗
PubMed2006

A comparison of complications of pregnancy and delivery in morbidly obese and non-obese women.

Morbid obesity in pregnancy is a growing problem and is having an impact on morbidity, mortality as well as significantly increasing antenatal and intra-partum costs of pregnancy care. The incidence of morbid obesity in pregnancy in our unit was 7.5% during the study period and this was associated with statistically significant increased maternal and perinatal morbidity. It also led to increased costs because of multidisciplinary management of the pregnancies, increased investigations and hospital stay when compared with normal weight pregnant women. Looking after morbidly obese pregnant women is an expensive undertaking, as the cost of the care of one morbidly obese pregnant woman and her baby is several times that of the normal weight woman. Health planners need to factor in these costs which are set to escalate given the predicted increase in the obese population in the UK.

Delivery, Obstetric↗
PubMed2006

Ability to control persistent asthma in obese versus non-obese children enrolled in an asthma-specific disease management program (breathmobile).

To determine if asthma control was more difficult to achieve in obese versus non-obese asthmatic children, retrospective analysis was performed on obese and non-obese Los Angeles inner-city children (2 to 18 years of age) with persistent asthma. No difference in time required to achieve control of asthma, ability to maintain control of asthma, baseline pulmonary functions, and number of controllers prescribed was found between the two groups. We conclude that in a Los Angeles inner-city pediatric population, obesity is not a factor in the ability to control asthma.

Adolescent↗
PubMed1983

Similarity of obesity indices in clinical studies of obese adults: a factor analytic study.

The similarity of measurements obtained with six commonly used obesity indices was assessed with correlational and factor analyses performed on data for 951 obese adults participating in a weight reduction study. Intercorrelations among the indices were found to be very high, with a mean of 0.96. A factor analysis of the six indices resulted in a single factor which accounts for 97% of the aggregate variance in the six indices. A factor analysis of the six indices plus height and weight resulted in two factors. The six indices loaded nearly perfectly on one factor and not at all on the second. Height loaded perfectly on the second factor. The results of these analyses constitute strong empirical evidence that the obesity indices are measuring the same thing and that factor is independent of height. Although anthropological or other special studies may necessitate the use of a particular index, these results suggest that it should make little difference which of the six indices is used in a clinical study of obesity with obese adults.

Analysis of Variance↗
PubMed1992

A survey of the opinions of obesity experts on the causes and treatment of obesity.

A survey of opinions on the causes and effectiveness of treatment of obesity was carried out on 50 physicians and scientists involved in obesity research. Responses were grouped by region (Europe, North America, and United Kingdom), sex, age (30-50 and greater than 50 y) and degree (MD or PhD). Genetic factors were considered the most important causes of obesity overall. Females viewed lack of physical activity, carbohydrate craving, and weight cycling as significantly more important causes than did their male colleagues and viewed exercise as a more effective treatment. There were regional variations in the assessment of the importance of metabolic defects and weight cycling as causes of obesity and in the usefulness of diet in the treatment of obesity. The older group of respondents rated low-fat diet more highly as a treatment than did their younger colleagues. All groups viewed serotonergic and thermogenic drugs as effective treatments whose usefulness would increase during the next 10 years.

Adult↗
PubMed1987

Reversal of obesity in the genetically obese fa/fa Zucker rat with an ephedrine/methylxanthines thermogenic mixture.

Administration of a thermogenic mixture of ephedrine, caffeine and theophylline to grossly obese (11-12 mo old) fa/fa Zucker rats led to a rapid decline in their body weight, which reached lean levels within 9-10 wk, and this postobese weight was maintained for another 5-6 wk. Compared to the no-drug obese controls (O-ND), food intake was reduced by 70% during the dynamic phase of weight loss and by 50% during the postobese period in the food-restricted animals (O-FR) and by about 40% during both phases in the ephedrine/methylxanthines (O-E/Mx) animals. Energy expenditure in the O-FR group was lower than in the O-E/Mx group by 25-33%. Analysis of body composition showed that body fat in both O-FR and O-E/Mx groups was much lower than in the O-ND group, by 2.5- and 4-fold, respectively, and body protein was lower by 50 and 28%, respectively. Thus, compared to the O-ND group, the fat:protein ratio was only 25% lower in the O-FR animals but was three times less in the O-E/Mx group. These findings demonstrate that in the fa/fa rat a mixture of ephedrine and methylxanthines reduces food intake but also minimizes the fall in metabolic rate that usually accompanies such an energy deficit, effects that led to a reversal of their gross obesity. The ability of ephedrine alone or in combination with methylxanthines to reverse obesity in animal models with dietary and hypothalamic etiologies is thus extended to the obesity resulting from the inheritance of a single-gene recessive defect.

Animals↗