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PubMed2004

Systematic review of the long-term effects and economic consequences of treatments for obesity and implications for health improvement.

OBJECTIVES: To undertake a systematic review of the long-term effects of obesity treatments on body weight, risk factors for disease, and disease. METHODS: The study encompassed three systematic reviews that examined different aspects of obesity treatments. (1) A systematic review of obesity treatments in adults where the methods of the Cochrane Collaboration were applied and randomised controlled trials (RCTs) with a follow-up of at least 1 year were evaluated. (2) A systematic epidemiological review, where studies were sought on long-term effects of weight loss on morbidity and/or mortality, and examined through epidemiological modelling. (3) A systematic economic review that sought reports with both costs and outcomes of treatment, including recent reports that assessed the cost-effectiveness of pharmaceutical and surgical interventions. A Markov model was also adopted to examine the cost-effectiveness of a low-fat diet and exercise intervention in adults with obesity and impaired glucose tolerance. RESULTS: The addition of the drugs orlistat or sibutramine was associated with weight loss and generally improved risk factors, apart from diastolic blood pressure for sibutramine. Metformin was associated with decreased mortality after 10 years in obese people with type 2 diabetes. Low-fat diets were associated with continuing weight loss for 3 years and improvements in risk factors, as well as prevention of type 2 diabetes and improved control of hypertension. Insufficient evidence was available to demonstrate the benefits of low calorie or very low calorie diets. The addition of an exercise or behaviour programme to diet was associated with improved weight loss and risk factors for at least 1 year. Studies combining low-fat diets, exercise and behaviour therapy suggested improved hypertension and cardiovascular disease. Family therapy was associated with improved weight loss for 2 years compared to individual therapy. There was insufficient evidence to conclude that individual therapy was more beneficial than group therapy. Weight lost more quickly (within 1 year), from the epidemiology review, may be more beneficial with respect to the risk of mortality. The effects of intentional weight loss need further investigation. Weight loss from surgical and non-surgical interventions for people suffering from obesity was associated with decreased risk of development of diabetes, and a reduction in low-density lipoprotein cholesterol, total cholesterol and blood pressure, in the long term. Targeting high-risk individuals with drugs or surgery was likely to result in a cost per additional life-year or quality-adjusted life-year (QALY) of no more than 13,000 British pounds. There was also suggestive evidence of cost saving from treatment of people with type 2 diabetes with metformin. Targeting surgery on people with severe obesity and impaired glucose tolerance was likely to be more cost-effective at 2329 British pounds per additional life-year. Economic modelling over 6 years for diet and exercise for people with impaired glucose tolerance was associated with a high initial cost per additional QALY, but by the sixth year the cost per QALY was 13,389 British pounds. Results did not include cost savings from diseases other than diabetes, and therefore may be conservative. CONCLUSIONS: The drugs orlistat and sibutramine appear beneficial for the treatment of adults with obesity, and metformin for obese patients with type 2 diabetes. Exercise and/or behaviour therapy appear to improve weight loss when added to diet. Low-fat diets with exercise, or with exercise and behaviour therapy are associated with the prevention of type 2 diabetes and hypertension. Long-term weight loss in epidemiological studies was associated with reduced risk of type 2 diabetes, and may be beneficial for cardiovascular disease. Low-fat diets and exercise interventions in individuals at risk of obesity-related illness are of comparable cost to drug treatments. Long-term pragmatic RCTs of obesity treatments in populations with obesity-related illness or at high risk of developing such illness are needed (to include an evaluation of risk factors, morbidity, quality of life and economic evaluations). Drug trials that include dietary advice, plus exercise and/or behaviour therapy are also needed. Research exploring effective types of exercise, diet or behaviour and also interventions to prevent obesity in adults is required.

Anti-Obesity Agents↗
PubMed2000

[Consumption of antihypertensive agents in obese patients: a cross-sectional study in a sample of 3,291 wage-earners in the Toulous region].

A cross-sectional study in a sample of 3,291 healthy workers was performed in May 1997 to assess the prevalence of obesity (BMI > or = 30 kg/m2) in a working population, and to compare prescription of antihypertensive drugs in obese and non obese subjects. Obesity was found in 7.4% (245) subjects and morbid obesity concerned 0.4% of the total sample (mean age 37.6 +/- 9.7 [SD] years, 52.4% of males). Risk of obesity was significantly associated with age, male sex, professional classes (higher in blue collars workers, lower in senior executive), business travels, atypical schedules, professional and private difficulties. Albeit the prevalence of drug users (49.7%) was similar whatever the BMI, obese subjects used a higher number of drugs than non obese (2.0 +/- 1.2 versus 1.6 +/- 0.9, p < 0.001). Risk of consumption of cardiovascular drugs was higher in obese than in non obese subjects (OR 2.9, 95% CI [2.2-4.1]). After adjustment on confounding factors, obesity increased specific drug use such as angiotensin converting enzyme inhibitors (OR 3.3, 95% CI [1.7-6.4]), beta-blocking agents (OR 2.83, 95% CI [1.01-8.01]), calcium channel blockers (OR 2.44, 95% CI [1.06-5.63]) or diuretics only in women (OR 5.7, 95% CI [2.1-16.3]). Prescribed antihypertensive drugs were different in obese (beta-blockers = angiotensin converting enzyme inhibitors > diuretics > calcium channels blockers) and non obese (angiotensin converting enzyme inhibitors > calcium channel blockers > diuretics > beta-blockers) subjects.

Adolescent↗
PubMedDate not supplied

[Prevalence of disability pension related to obesity in Iceland 1992-2004].

OBJECTIVES: To investigate changes in the prevalence of disability pension related to obesity in Iceland from 1992 to 2004. MATERIAL AND METHODS: Data were obtained from the disability register of the State Social Security Institute and Statistics Iceland for the years 1992 and 2004. Prevalence of disability pension related to obesity and of disability pension in general was calculated for both years. Statistical significance was assessed by calculating chi square and standardized risk ratios. RESULTS: From 1992 to 2004 the number of recipients of disability pension with obesity as a primary diagnosis increased from 37 to 111, amounting to 183% increase for females and 263% for males. This increase is significantly greater than the increase in disability pension in general during this period. Age standardized risk ratio showed increased disability related to obesity for both genders. Among males it was greater than the general increase in disability, while among females it was less. There was a significantly greater increase in disability related to obesity in areas outside the capital compared with Reykjavík and surrounding areas among females. The increase in disability related to obesity far surpasses the increase in obesity in the population, according to population surveys, suggesting that severe and morbid obesity may be particularly on the rise. CONCLUSION: There has been a significant increase in the prevalence of disability pension related to obesity in Iceland from 1992 to 2004. It is possible that increased social awareness of obesity during the study period has influenced diagnostic habits of physicians and thus increased the use of obesity as a diagnosis in medical certificates and disability assessment. In all likelihood, however, there has been an increase in disabling obesity in Iceland, indicating that obesity is an increasing public health problem demanding appropriate intervention.

Chi-Square Distribution↗
PubMed1991

[Investigation of the relationships between zinc and obesity].

Zinc is known to be an essential trace metal which is necessary for health and growth, and is also essential for the function and activity of over 200 metalloenzymes. A relationship between zinc and obesity was first found in obese patients and obese mice (genetically and dietary obese) to that the obese had lower blood zinc levels than their lean controls, and the zinc level was inversely related to the degree of obesity. The therapeutic effect of zinc on obesity is still a controversial subject. This study was to investigate the alterations of tissues zinc distribution, dietary zinc effect in obese mice, and the interactive combinations of zinc and endocrine factors in obese patients. Zinc and body fat contents were determined by atomic absorption spectrometer and gravimetrically, respectively. The results indicated that dietary zinc treatment increased body fat deposition in obese mice. Obese mice carried markedly low zinc levels in most of the peripheral tissues, but retained a great amount of zinc in liver and adipose tissues compared with lean mice. Clinically, zinc was found to be correlated with thyroid hormone conversion and insulin resistance. Although the true metabolic role of zinc in obesity is still obscure, the relationships between zinc, endocrine factors, and neurotransmitters, and interactions with other trace metals are needed to throw light on the subject. These approaches to thermoregulation and metabolic mechanisms of obesity and diabetes mellitus may be of great interest in the future.

Adult↗
PubMed1998

Management of obesity in NIDDM (non-insulin-dependent diabetes mellitus).

Obesity is common in NIDDM; in a cohort of 314 diabetics in Singapore, 44.3% are overweight. Management of obesity in diabetics differs from that in non-diabetics in that it is more urgent; weight maintenance is more difficult and hypoglycaemic medication may cause weight changes. Like in the non-diabetic, management of obesity in diabetic requires a pragmatic and realistic approach. A team approach is required: the help of the nurse educator, the dietitian, behaviour modification therapist, exercise therapist etc are required. A detailed history, careful physical examination and relevant investigations are required to assess the severity of the diabetic state and to exclude an occasional underlying cause of the obesity in the obese NIDDM. Weight loss is urgent in the obese NIDDM, especially those with android obesity. There must be a reduction in caloric intake. Weight loss leads to improvement in the glucose tolerance, insulin sensitivity, reduction in lipid levels and fall in blood pressure in the hypertensive. Exercise is of limited value except in the younger obese NIDDM. Metformin is the hypoglycaemic drug of choice as it leads to consistent weight reduction. The sulphonylureas may cause weight gain. Insulin should be avoided where possible as it causes further weight gain. Other hypoglycaemic agents include Glucobay (alpha-glucosidase inhibitor) and Troglitazone (insulin sensitizer) which do not alter the weight. Orlistat (lipase inhibitor) is promising as it causes reduction of weight, blood-glucose and lipid levels. Anti-obesity drugs (noradrenergic and serotonergic agents) have modest effects on weight reduction in the obese NIDDM; a widely use preparation, Dexfenfluramine (Adifax) has been withdrawn because of side effects. Surgery such as gastric plication is the last resort in treating the morbidly obese NIDDM. The discovery of leptin in 1994 has led to intense research into energy homeostasis in obesity; hopefully this will lead to better treatment of obesity in diabetics and non-diabetics.

Anti-Obesity Agents↗
PubMed2006

Binge-eating disorder as a distinct familial phenotype in obese individuals.

CONTEXT: Binge-eating disorder (BED)-a syndrome that only recently has attracted scientific attention-is often seen in obese individuals, especially those with severe obesity. However, it remains unclear whether BED represents an etiologically distinct behavioral phenotype of obesity or simply a nonspecific eating pattern sometimes seen in obese individuals. OBJECTIVE: To test whether BED aggregates in families independently of obesity, and if so, whether familial factors for BED also independently increase the risk of obesity. DESIGN, PATIENTS, AND SETTING: Blinded family interview study of overweight or obese probands with (n = 150) and without (n = 150) BED, and their first-degree relatives (n = 888) in a community setting evaluated between October 2002 and July 2004. MAIN OUTCOME MEASURES: Lifetime diagnosis of BED; current and highest lifetime body mass index (calculated as the weight in kilograms divided by the square of the height in meters). RESULTS: Binge-eating disorder aggregated strongly in families independently of obesity (odds ratio, 2.2; 95% confidence interval, 1.4-3.6; P<.001). Furthermore, relatives of probands with BED displayed a markedly higher prevalence of severe obesity in adulthood (body mass index >/=40) than relatives of probands without BED even when controlling for proband body mass index (odds ratio, 2.5; 95% confidence interval, 1.4-4.4; P = .002). CONCLUSIONS: Binge-eating disorder is a familial disorder caused in part by factors distinct from other familial factors for obesity. Furthermore, these BED-specific familial factors may independently increase the risk of obesity, especially severe obesity. It follows that targeted interventions capable of preventing or treating traits influenced by these BED-specific familial factors could reduce the public health burden of obesity.

Adolescent↗
PubMed2003

Television watching and other sedentary behaviors in relation to risk of obesity and type 2 diabetes mellitus in women.

CONTEXT: Current public health campaigns to reduce obesity and type 2 diabetes have largely focused on increasing exercise, but have paid little attention to the reduction of sedentary behaviors. OBJECTIVE: To examine the relationship between various sedentary behaviors, especially prolonged television (TV) watching, and risk of obesity and type 2 diabetes in women. DESIGN, SETTING, AND PARTICIPANTS: Prospective cohort study conducted from 1992 to 1998 among women from 11 states in the Nurses' Health Study. The obesity analysis included 50 277 women who had a body mass index (BMI) of less than 30 and were free from diagnosed cardiovascular disease, diabetes, or cancer and completed questions on physical activity and sedentary behaviors at baseline. The diabetes analysis included 68 497 women who at baseline were free from diagnosed diabetes mellitus, cardiovascular disease, or cancer. MAIN OUTCOME MEASURES: Onset of obesity and type 2 diabetes mellitus. RESULTS: During 6 years of follow-up, 3757 (7.5%) of 50 277 women who had a BMI of less than 30 in 1992 became obese (BMI > or =30). Overall, we documented 1515 new cases of type 2 diabetes. Time spent watching TV was positively associated with risk of obesity and type 2 diabetes. In the multivariate analyses adjusting for age, smoking, exercise levels, dietary factors, and other covariates, each 2-h/d increment in TV watching was associated with a 23% (95% confidence interval [CI], 17%-30%) increase in obesity and a 14% (95% CI, 5%-23%) increase in risk of diabetes; each 2-h/d increment in sitting at work was associated with a 5% (95% CI, 0%-10%) increase in obesity and a 7% (95% CI, 0%-16%) increase in diabetes. In contrast, standing or walking around at home (2 h/d) was associated with a 9% (95% CI, 6%-12%) reduction in obesity and a 12% (95% CI, 7%-16%) reduction in diabetes. Each 1 hour per day of brisk walking was associated with a 24% (95% CI, 19%-29%) reduction in obesity and a 34% (95% CI, 27%-41%) reduction in diabetes. We estimated that in our cohort, 30% (95% CI, 24%-36%) of new cases of obesity and 43% (95% CI, 32%-52%) of new cases of diabetes could be prevented by adopting a relatively active lifestyle (<10 h/wk of TV watching and > or =30 min/d of brisk walking). CONCLUSIONS: Independent of exercise levels, sedentary behaviors, especially TV watching, were associated with significantly elevated risk of obesity and type 2 diabetes, whereas even light to moderate activity was associated with substantially lower risk. This study emphasizes the importance of reducing prolonged TV watching and other sedentary behaviors for preventing obesity and diabetes.

Adult↗
PubMed2004

Prevalence of overweight and obesity among US children, adolescents, and adults, 1999-2002.

CONTEXT: The prevalence of overweight and obesity has increased markedly in the last 2 decades in the United States. OBJECTIVE: To update the US prevalence estimates of overweight in children and obesity in adults, using the most recent national data of height and weight measurements. DESIGN, SETTING, AND PARTICIPANTS: As part of the National Health and Nutrition Examination Survey (NHANES), a complex multistage probability sample of the US noninstitutionalized civilian population, both height and weight measurements were obtained from 4115 adults and 4018 children in 1999-2000 and from 4390 adults and 4258 children in 2001-2002. MAIN OUTCOME MEASURE: Prevalence of overweight (body mass index [BMI] > or =95th percentile of the sex-specific BMI-for-age growth chart) among children and prevalence of overweight (BMI, 25.0-29.9), obesity (BMI > or =30.0), and extreme obesity (BMI > or =40.0) among adults by sex, age, and racial/ethnic group. RESULTS: Between 1999-2000 and 2001-2002, there were no significant changes among adults in the prevalence of overweight or obesity (64.5% vs 65.7%), obesity (30.5% vs 30.6%), or extreme obesity (4.7% vs 5.1%), or among children aged 6 through 19 years in the prevalence of at risk for overweight or overweight (29.9% vs 31.5%) or overweight (15.0% vs 16.5%). Overall, among adults aged at least 20 years in 1999-2002, 65.1% were overweight or obese, 30.4% were obese, and 4.9% were extremely obese. Among children aged 6 through 19 years in 1999-2002, 31.0% were at risk for overweight or overweight and 16.0% were overweight. The NHANES results indicate continuing disparities by sex and between racial/ethnic groups in the prevalence of overweight and obesity. CONCLUSIONS: There is no indication that the prevalence of obesity among adults and overweight among children is decreasing. The high levels of overweight among children and obesity among adults remain a major public health concern.

Adolescent↗
PubMed1993

Treatment of obese female and male SHHF/Mcc-fa(cp) rats with antihypertensive drugs, nifedipine and enalapril: effects on body weight, fat distribution, insulin resistance and systolic pressure.

Little is known about the effects of common antihypertensive drugs in obese, insulin-resistant females. Nine-month-old obese female SHHF/Mcc-fa(cp) rats that received either nifedipine, a calcium channel antagonist, or enalapril, an angiotensin-converting-enzyme inhibitor, for three months were compared with untreated SHHF/Mcc-fa(cp) rats (controls). After one month, nifedipine significantly decreased body weight in obese females compared to either enalapril or controls. After three months of treatment, total, abdominal, and subcutaneous fat masses were decreased in obese females given nifedipine compared to either enalapril or controls. Enalapril treatment was associated with a redistribution of fat mass from abdominal to subcutaneous depots. Nifedipine reduced plasma triglyceride and fasting glucose levels and improved insulin response to an oral glucose load in obese females, whereas enalapril did not appear to affect glycemic control. Systolic pressure was not significantly decreased until after two months of treatment with nifedipine or three months of treatment with enalapril in obese females and may have coincided with improvement in insulin-resistance. Similarly, plasma atrial natriuretic peptide concentrations were significantly lower in obese females given nifedipine. To determine how obese males responded to a calcium channel antagonist, six-month-old obese male SHHF/Mcc-fa(cp) rats were treated for three months with either nifedipine or placebo (controls). Nifedipine-treated obese males showed a mild but significant decrease in weight gain that was due to a decrease in fat deposition in both subcutaneous and abdominal depots and systolic blood pressure was significantly reduced after one month of treatment. Nifedipine did not affect other plasma biochemical parameters in obese males. In conclusion, nifedipine improved systolic pressure and glycemic control in obese female SHHF/Mcc-fa(cp) rats, effects that may be associated with a marked loss in body weight and fat mass and improved lipid metabolism. Nifedipine-treated obese males exhibited only a diminished weight gain that was not associated with changes in diabetic characteristics.

Animals↗
PubMed1993

Insulin secretion in hypothalamic obesity: diurnal variation and the effect of naloxone.

This paper has tested the hypothesis that patients with hypothalamic obesity have altered mechanisms controlling insulin secretion when compared to obese patients without hypothalamic injury. Fasting glucose and insulin values were significantly higher in the morning than in the afternoon in the six control obese patients, but there was no diurnal difference in the six patients with hypothalamic obesity (n=6). The control obese subjects showed a diurnal variation in glucose-stimulated insulin secretion, whereas the patients with hypothalamic obesity did not, suggesting that hypothalamic injury had destroyed diurnal rhythms. Naloxone, an opioid antagonist, acutely suppressed fasting insulin in the six patients with essential obesity but had little effect on fasting insulin in the three patients with hypothalamic obesity or in five normal-weight controls. Naloxone increased insulin sensitivity in the obese control patients, but did not affect either insulin secretion or insulin sensitivity in patients with hypothalamic obesity or in normal weight subjects. Our results support the conclusion that hypothalamic obesity disrupts diurnal rhythms, with the suggestion that opioid peptides affect insulin secretion differently in patients with essential obesity as compared to normal weight subjects or those with hypothalamic obesity.

Adolescent↗
PubMed1995

Obesity and malnutrition in a Shantytown population in the city of São Paulo, Brazil.

To investigate the prevalence of obesity and malnutrition in the poor Brazilian population we conducted a survey on the socioeconomic and nutritional status of 535 families (comprising 2,411 individuals) living in shantytowns in the city of São Paulo. There was a 30% prevalence of malnutrition in the children, with chronic malnutrition as the most predominant problem. The prevalence of obesity was 6.4% in boys and 8.7% in girls. Overweight and obesity associated with stunting was found in 5.8% of boys and 6.8% girls. Adolescents showed a higher prevalence of malnutrition when weight-for-age distribution was used (boys 46.4%, girls 40.2%), but a right deviation in the distribution was observed with an increase in obesity and a decrease of malnutrition was observed (obesity was 21% in girls and 8.8% in boys; malnutrition was 15.5% in boys and 12.6% in girls) when the weight-for-height adjustment was made. Stunting was the most predominant type of malnutrition in both sexes. Obesity associated with stunting was more common than obesity without stunting, both in younger children and adolescents. Adults had a higher prevalence of obesity than malnutrition according to both the Metropolitan Life Insurance tables (1.7% of undernutrition, 16.7% of overweight, and 14.1% of obesity) and Body Mass Index (8.5% of undernutrition, 21.9% of overweight, and 14.6% of obesity). There was an increase in the percentage of obese children when at least one adult in the family was obese and an increased percentage of malnourished children when undernourished adults were present in the family. Obesity among the adults of the family decreased the occurrence of malnutrition among the children.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Genetic aspects of susceptibility to obesity and related dyslipidemias.

Obesity has a multifactorial origin. However, although environmental variables undoubtedly play a role in the development of obesity, it is now clear that genetic variation is also involved in the determination of an individual's susceptibility to body fat accumulation. In addition, it is also widely accepted that obesity is not a single homogeneous phenotype. It is also heterogeneous regarding its causes and metabolic complications. The regional distribution of body fat appears to be an important correlate of the metabolic complications that have been related to obesity. Due to their higher accumulation of abdominal fat, men are generally more at risk for the metabolic complications of obesity than women whereas some obese women, with large gluteal-femoral adipose depots may have a cosmetic problem which may not necessarily require medical intervention. Several studies have been conducted to understand the mechanisms by which abdominal obesity is related to diabetes, hypertension and cardiovascular disease. It appears that the increased risk of abdominal obesity is the result of complex hormonal and metabolic interactions. Studies in genetic epidemiology have shown that both total body fatness and the regional distribution of body fat have a significant genetic component. Standardized intervention studies using an identical twin design have shown that individuals that have the same genetic background tend to show similar changes in body fat and in plasma lipoprotein levels when exposed to standardized caloric excess or energy restriction. Finally, although abdominal obesity is a significant risk factor for cardiovascular disease, not every abdominal obese subject will experience metabolic complications, suggesting that some obese individuals may be more susceptible than others. Variation in several genes relevant to lipid and lipoprotein metabolism may alter the relation of abdominal obesity to dyslipoproteinemias. Abdominal obesity should therefore be considered as a factor that exacerbates an individual's susceptibility to cardiovascular disease.

Adipose Tissue↗
PubMedDate not supplied

Gastric inhibitory polypeptide (GIP) hypersecretion in obesity depends on meal size and is not related to hyperinsulinemia.

The response of immunoreactive gastric inhibitory polypeptide (IR-GIP), immunoreactive insulin (IRI) and immunoreactive C-peptide (IR-C-peptide) to the ingestion of mixed liquid test meals containing 1031 kcal (550 ml) and 422 kcal was studied in 17 obese and 17 normal weight control subjects. When the 422 kcal load was ingested in a volume of 550 ml, the plasma IR-GIP response was significantly greater than in a volume of 225 ml at 15 and 30 min in lean and obese subjects, but the total integrated IR-GIP response was not significantly different between the obese and lean group. Also intraduodenal infusion of 150 ml (280 kcal) of the test meal elicited identical plasma IR-GIP concentrations in lean and obese subjects. An exaggerated IR-GIP response in obese subjects was seen only following the 1031 kcal load (integrated IR-GIP response: 23.6 +/- 1.9 in lean subjects vs 50.3 +/- 3.8 nmol/l/180 min in obese subjects; p less than 0.01). The IRI response was always significantly greater in obese than in lean subjects and not related to the GIP response. Fasting plasma IR-C-peptide levels were significantly elevated in obese subjects (lean: 0.52 +/- 0.04; obese: 1.42 +/- 0.12 nmol/l; p less than 0.005), but the postprandial integrated IR-C-peptide responses in the obese and lean group were identical, indicating decreased hepatic insulin extraction in obesity. It is concluded that an exaggerated IR-GIP response in obesity occurs only after ingestion of a high calorie meal probably as consequence of an increased gastric emptying rate and that the hyperinsulinemic response of obese subjects is not attributable to GIP hypersecretion.

Blood Glucose↗
PubMed2005

Plasma total homocysteine level and its association with carotid intima-media thickness in obesity.

BACKGROUND: Elevated plasma concentrations of total homocysteine (tHcy) and obesity are risk factors for cardiovascular disease. The relationship between hyperhomocysteinemia and obesity has not been totally elucidated. OBJECTIVE: The first aim of the study was to investigate whether anthropometric measurements and insulin resistance contribute to the variation in homocysteine levels in obese adults. Our second aim was to determine if any relationship exists between the carotid intima-media thickness (IMT) and plasma tHcy levels in obese subjects without traditional cardiovascular risk factors. MATERIAL AND METHODS: Fifty-five obese (15 male, 40 female) and 30 (11 male, 19 female) age- and sex-matched apparently healthy volunteers were included. Exclusion criteria were smoking, hypertension, diabetes, vitamin ingestion, hyperlipidemia, renal failure, liver disease, pregnancy, menopause and secondary obesity such as Cushing's syndrome, hypothyroidism. tHcy, folate, vitamin B12 levels, fasting insulin, glucose, total cholesterol, triglycerides, HDL, LDL particles, uric acid, creatinine and creatinine clearance were measured. Non-invasive ultrasound measurements of carotid IMT were performed. RESULTS: tHcy levels and carotid IMT were comparable between obese and non-obese subjects. Waist/hip ratio (WHR) was related to tHcy and carotid IMT. Hyperhomocysteinemic subjects (tHcy >19.2 micromol/l) had greater WHR than normo-homocysteinemic subjects. Both tHcy levels and carotid IMT were higher in male subjects both in obese and non-obese subjects. No association was observed between insulin resistance and tHcy and carotid IMT. Renal function and abdominal obesity were significant predictors of plasma tHcy levels. CONCLUSIONS: We concluded that, in obese subjects who are free from atherosclerosis and impaired renal function, plasma tHcy levels do not differ from healthy subjects. Plasma tHcy concentrations are not related to carotid IMT in obese subjects during the non-atherogenic stage. Although no significant difference was observed between insulin-resistant and insulin-sensitive subjects compared to the plasma tHcy levels, the relationship between tHcy levels and some components of the insulin resistance syndrome may support the opinion that tHcy may be considered a component of the insulin resistance syndrome.

Adult↗
PubMed2000

Aetiology of overweight and obesity in children and adolescents.

UNLABELLED: The epidemic diffusion of obesity in industrialised countries has promoted research on the aetiopathogenesis of this disorder. The purpose of this review is to focus mainly on the contribution that European research has made to this field. Available evidence suggests that obesity results from multiple interactions between genes and environment. Parents obesity is the most important risk factor for childhood obesity. Twin, adoption, and family studies indicated that inheritance is able to account for 25% to 40% of inter-individual difference in adiposity. Single gene defects leading to obesity have been discovered in animals and, in some cases, confirmed in humans as congenital leptin deficiency or congenital leptin receptor deficiency. However, in most cases, genes involved in weight gain do not directly cause obesity but they increase the susceptibility to fat gain in subjects exposed to a specific environment. Both genetic and environmental factors promote a positive energy balance which cause obesity. The relative inefficiency of self-adapting energy intake to energy requirements is responsible for fat gain in predisposed individuals. The role of the environment in the development of obesity is suggested by the rapid increase of the prevalence of obesity accompanying the rapid changes in the lifestyle of the population in the second half of this century. Early experiences with food, feeding practices and family food choices affect children's nutritional habits. In particular, the parents are responsible for food availability and accessibility in the home and they affect food preferences of their children. Diet composition, in particular fat intake, influences the development of obesity. The high energy density and palatability of fatty foods as well as their less satiating properties promotes food consumption. TV viewing, an inactivity and food intake promoter, was identified as a relevant risk factor for obesity in children. Sedentarity, i.e. a low physical activity level, is accompanied by a low fat oxidation rate in muscle and a low fat oxidation rate is a risk factor of fat gain or fat re-gain after weight loss. CONCLUSION: Further research is needed to identify new risk factors of childhood obesity, both in the genetic and environmental areas, which may help to develop more effective strategies for the prevention and treatment of obesity.

Adolescent↗
PubMed2005

Hypoadiponectinaemia and high risk of type 2 diabetes are associated with adiponectin-encoding (ACDC) gene promoter variants in morbid obesity: evidence for a role of ACDC in diabesity.

AIMS/HYPOTHESIS: Morbid obesity (BMI>40 kg/m(2)) affecting 0.5-5% of the adult population worldwide is a major risk factor for type 2 diabetes. We aimed to elucidate the genetic bases of diabetes associated with obesity (diabesity), and to analyse the impact of corpulence on the effects of diabetes susceptibility genes. METHODS: We genotyped known single nucleotide polymorphisms (SNPs) in the adiponectin-encoding adipocyte C1q and collagen-domain-containing (ACDC) gene (-11,391G>A, -11,377C>G, +45T>G and +276G>T), the peroxisome proliferator-activated receptor gamma (PPARG) Pro12Ala SNP and ACDC exon 3 variants in 703 French morbidly obese subjects (BMI 47.6+/-7.4 kg/m(2)), 808 non-obese subjects (BMI<30 kg/m(2)) and 493 obese subjects (30< or =BMI<40 kg/m(2)). RESULTS: Two 5'-ACDC SNPs -11,391G>A, -11,377C>G were associated with adiponectin levels (p=0.0003, p=0.008) and defined a "low-level" haplotype associated with decreased adiponectin levels (p=0.0002) and insulin sensitivity (p=0.01) and with a risk of type 2 diabetes that was twice as high (p=0.002). In contrast, the prevalence of the PPARG Pro12Ala was identical in diabetic and normoglycaemic morbidly obese subjects. The PPARG Pro12 allele only displayed a trend of association with type 2 diabetes in the non-obese group. ACDC exon 3 variants were associated with type 2 diabetes in the non-obese group only (odds ratio 7.85, p<0.0001). In contrast, the 5'-ACDC "low-level" haplotype was associated with type 2 diabetes in obese and morbidly obese subjects (odds ratio 1.73 and 1.92) but not in non-obese individuals. CONCLUSIONS/INTERPRETATION: These data clarify the contribution of the 5'-ACDC SNPs to the risk of diabesity. Their interaction with corpulence suggests for the first time a different genetic profile of type 2 diabetes in morbidly obese patients compared with in less obese individuals.

Adiponectin↗
PubMed2006

WNT10B mutations in human obesity.

AIMS/HYPOTHESIS: Recent studies suggest that wingless-type MMTV integration site family, member 10B (WNT10B) may play a role in the negative regulation of adipocyte differentiation in vitro and in vivo. In order to determine whether mutations in WNT10B contribute to human obesity, we screened two independent populations of obese subjects for mutations in this gene. SUBJECTS AND METHODS: We studied 96 subjects with severe obesity of early onset (less than 10 years of age) from the UK Genetics of Obesity Study and 115 obese Italian subjects of European origin. RESULTS: One proband with early-onset obesity was found to be heterozygous for a C256Y mutation, which abrogated the ability of WNT10B to activate canonical WNT signalling and block adipogenesis and was not found in 600 control alleles. All relatives of the proband who carried this allele were either overweight or obese. Three other rare missense variants were found in obese probands, but these did not clearly cosegregate with obesity in family studies and one (P301S), which was found in three unrelated subjects with early-onset obesity, had normal functional properties. CONCLUSIONS/INTERPRETATION: These mutations represent the first naturally occurring missense variants of WNT10B. While the pedigree analysis in the case of C256Y WNT10B does not provide definitive proof of a causal link of this variant with obesity, the finding of a non-functioning WNT10B allele in a human family affected by obesity should encourage further study of this gene in other obese populations.

Adipocytes↗
PubMed1983

Neuromechanical properties in obese patients during carbon dioxide rebreathing.

During hypercapnia-induced hyperventilation, obese patients with a prior history of alveolar hypoventilation appear to have significantly more blunted ventilatory response than simply obese patients who never retained carbon dioxide. In addition, these patients with former obesity-hypoventilation syndrome have decreased neuromuscular responses as measured by way of the mouth occlusion technique when compared with either the patients with simple obesity or normal subjects. The patients with simple obesity appear to have augmented responses in comparison with normal subjects. Simple mechanical considerations and baseline breathing variables failed to distinguish the simple obesity group from the group with former obesity-hypoventilation syndrome. Thus, the decreased neuromuscular responsiveness to carbon dioxide (mouth-occlusion pressure/end-tidal carbon dioxide pressure) among the group with former obesity-hypoventilation syndrome when compared with that in the group with simple obesity is a consequence of a blunted neural (central) drive, and not due to any apparent worse mechanical limitations. The augmented mouth-occlusion pressure/end-tidal carbon dioxide pressure and increased integrated, rectified electromyographic signal of the diaphragm found in the group with simple obesity presumably reflect their attempt to maintain ventilatory homeostasis in the presence of severe respiratory loads. Neuromechanical coupling values, as reflected in the integrated electromyographic signal of the diaphragm versus transdiaphragmatic pressure and mouth-occlusion pressure versus mean inspiratory flow, are identical in the two groups. On the basis of these studies, it would appear that although mechanical loads put all obese patients at a disadvantage, the addition of an acute extra load on the respiratory system produces the obesity-hypoventilation syndrome in those obese persons who have truly blunted central hypercapnic responses.

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