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PubMed2005

The effect of orlistat-induced weight loss on interleukin-6 and C-reactive protein levels in obese subjects.

OBJECTIVE: Inflammation plays a major role in the pathogenesis of atherosclerosis. Obesity is an independent risk factor for cardiovascular disease, which may be mediated by increased secretion of proinflammatory cytokines by adipose tissue. The aim of this study is to investigate changes in the inflammatory markers interleukin-6 (IL-6) and high-sensitivity C-reactive protein (hs-CRP) during weight reduction with orlistat treatment in obese patients. METHODS AND RESULTS: Thirty-six obese (BMI: 36.1 +/- 3.4 kg/m2) and II non-obese (BMI: 22.9 +/- 1.7 kg/m2) subjects were studied. IL-6 and hs-CRP levels were evaluated at baseline. In obese subjects after treatment of orlistat 120 mg three times daily for 6 months, IL-6 and hs-CRP levels were repeated. Levels of circulating IL-6 (p < 0.05) and hs-CRP (p < 0.01) were significantly higher in the obese group than in the non-obese group. Plasma IL-6 (r = 0.29 and p < 0.05) and CRP (r = 0.35 and p < 0.05) concentrations correlated positively with the level of obesity assessed by BMI at baseline. After 6 months of orlistat treatment in obese subjects, the mean weight of the patients decreased by 6.8 kg, the BMI by 3.2 kg/m2. Compared with baseline, weight loss was associated with significant reductions of IL-6 (p < 0.001) and hs-CRP (p < 0.001) levels. CONCLUSION: In summary plasma IL-6 and hs-CRP levels were increased in obese patients. Orlistat-induced weight reduction was associated with decreasing levels of both IL-6 and hs-CRP in obese subjects. Because inflammatory mediators may be directly involved in atherogenesis, this would suggest that interventions to reduce IL-6 and CRP levels could be cardioprotective.

Adult↗
PubMed2002

Positional candidate gene analysis of Lim domain homeobox gene (Isl-1) on chromosome 5q11-q13 in a French morbidly obese population suggests indication for association with type 2 diabetes.

The Lim domain homeobox gene (Isl-1) is a positional candidate gene for obesity that maps on chromosome 5q11-q13, a locus linked to BMI and leptin levels in French Caucasians. Isl-1 might be involved in body weight regulation and glucose homeostasis via the activation of proglucagon gene expression, which encodes for glucagon and glucagon-like peptides. By mutation screening of 72 obese subjects, we identified three single-nucleotide polymorphisms (SNPs) in the Isl1 gene. The allele frequencies in the morbidly obese group did not differ from that of the control group. In the obese group, the -47G allele was associated with a decreased risk of type 2 diabetes (odds ratio 0.41, P = 0.019). The AG bearers displayed a higher maximal BMI than the AA bearers in the whole obese group (P = 0.026) as well as in the type 2 diabetic obese subgroup (P = 0.014). In obese families, this allele was not preferentially transmitted from heterozygous parents to their obese siblings, indicating that Isl-1 does not contribute to the linkage with obesity on 5cen-q. However, in French Caucasian morbidly obese subjects, the Isl1-47A-->G SNP may modulate the risk for type 2 diabetes and may increase body weight in diabetic morbidly obese subjects.

Adult↗
PubMed2000

[Monogenic forms of obesity: from mice to human].

The cloning of five rodent obesity genes has constituted a major advance in our understanding of body weight homeostasis. Breakthroughs in human molecular genetics have identified mutations disrupting either rodent homologue/analogue genes or genes involved in the same pathways in obese patients. Three rare cases of human morbid obesity of early onset associated with hypogodatropic hypogodanism are due to mutations in the leptin and the leptin receptor genes. These studies have confirmed that leptin plays not only a crucial role in the control of body weight in the human but also in several endocrine functions. Other Human obesity syndromes are linked to mutations in the genes encoding brain-expressed targets of leptin, particularly some key components of the melanocortin system. Patients compound heterozygous for mutations in the POMC gene display severe obesity of early onset, congenital adrenal insufficiency and red hair. Another genetic cause of obesity is due to mutation in the Proconvertase gene (PC1), the enzyme required for the cleavage of POMC into ACTH and alpha MSH, and also of Proinsulin to insulin. The subject compound heterozygous for the PC1 mutation displays besides obesity, a partial ACTH deficiency, elevated POMC and late post absorptive hypoglycemia due to the accumulation of high pro-insulinemia. Contrasting largely with these rare syndromic forms of obesity, several mutations located in the melanocortin 4 receptor gene have been showed to cause an early onset dominant form of obesity with no other associated abnormalities indifferent populations. These mutations in MC4-R could represent a "frequent" cause of common monogenic forms of obesity in human. More generally, these researches into human obesity have opened new exciting understandings in some of the pathways regulating body fat mass.

Adrenocorticotropic Hormone↗
PubMed2002

B vitamins, vitamin C and hematological measurements in overweight and obese Thais in Bangkok.

The dynamic changes of socio-economics leading to the industrialisation of countries are known to affect lifestyle and nutritional behaviours of the population. Review of the literature on the prevalence of obesity showed increasing numbers of the overweight and obese during the past decade. However, information on health and nutritional status of the obese in Thailand has not been widely publicized. This study reveals the vitamin status and hematological picture in 270 overweight and obese Thais in Bangkok, Thailand, compared with 175 normal subjects. No statistically significant differences in haemoglobin and hematocrit were observed in the overweight compared with the control subjects. The prevalence of anaemia was 9.8 per cent among male and 17.2 per cent among female overweight and obese subjects compared with 2.6 per cent and 21.2 per cent in male and female normal controls using the cut-off point of haemoglobin concentration as an indicator of anaemia. Prevalence of hypertension was exhibited in both male and female overweight and obese subjects. Even if there were no statistically significant differences in vitamin B1, B2 and B6 in overweight and obese subjects compared with the controls, high percentages of vitamin C and vitamin B2 deficiencies were observed. Vitamin B2 deficiency was detected in 19.7 per cent of overweight and obese males as well as in 28.7 per cent of overweight and obese females using glutathione reductase activity coefficient (alpha EGR) < 1.5 as the cut-off point. However, clinical signs of vitamin B2 deficiencies were rare. There was also a high percentage of vitamin C (antioxidant vitamin) deficiency in 51.5 per cent of the overweight and obese subjects and 41.7 per cent of the controls, respectively. The results suggest more attention should be paid to health study and nutritional problems for the overweight and obese population, especially concerning vitamins and oxidative stress. Further research is still needed in these aspects.

Adolescent↗
PubMed2004

The association between obesity and screening mammography accuracy.

BACKGROUND: Obesity is increasing among American women, especially as they age. The influence of obesity on the accuracy of screening mammography has not been studied extensively. METHODS: We analyzed 100 622 screening mammography examinations performed on members of a nonprofit health plan. The relationship between body mass index (weight in kilograms divided by the square of height in meters) and measures of screening accuracy was assessed. Body mass index was categorized as underweight or normal weight (<25), overweight (25-29), obesity class I (30-34), and obesity classes II to III (> or =35). RESULTS: Compared with underweight or normal weight women, overweight and obese women were more likely to be recalled for additional tests after adjusting for important covariates, including age and breast density (overweight odds ratio [OR], 1.17; 95% confidence interval [CI], 1.11-1.23); obesity class I OR, 1.27; 95% CI, 1.19-1.35; obesity classes II-III OR, 1.31; 95% CI, 1.22-1.41). As body mass index increased, women were more likely to have lower specificity (overweight OR, 0.86; 95% CI, 0.81-0.90; obesity class I OR, 0.79; 95% CI, 0.74-0.84; and obesity classes II-III OR, 0.77; 95% CI, 0.71-0.82). No statistically significant differences were noted in sensitivity. Adjusted receiver operating characteristic analysis showed statistically significant improvement in the area under the curve (AUC) for underweight or normal weight women (AUC = 0.941) vs overweight women (AUC = 0.916, P =.02) and underweight or normal weight women vs obesity classes II and III women (AUC = 0.904, P =.02). CONCLUSIONS: Obese women had more than a 20% increased risk of having false-positive mammography results compared with underweight and normal weight women, although sensitivity was unchanged. Achieving a normal weight may improve screening mammography performance.

Adult↗
PubMed1999

Annual deaths attributable to obesity in the United States.

CONTEXT: Obesity is a major health problem in the United States, but the number of obesity-attributable deaths has not been rigorously estimated. OBJECTIVE: To estimate the number of deaths, annually, attributable to obesity among US adults. DESIGN: Data from 5 prospective cohort studies (the Alameda Community Health Study, the Framingham Heart Study, the Tecumseh Community Health Study, the American Cancer Society Cancer Prevention Study I, and the National Health and Nutrition Examination Survey I Epidemiologic Follow-up Study) and 1 published study (the Nurses' Health Study) in conjunction with 1991 national statistics on body mass index distributions, population size, and overall deaths. SUBJECTS: Adults, 18 years or older in 1991, classified by body mass index (kg/m2) as overweight (25-30), obese (30-35), and severely obese (>35). MAIN OUTCOME MEASURE: Relative hazard ratio (HR) of death for obese or overweight persons. RESULTS: The estimated number of annual deaths attributable to obesity varied with the cohort used to calculate the HRs, but findings were consistent overall. More than 80% of the estimated obesity-attributable deaths occurred among individuals with a body mass index of more than 30 kg/m2. When HRs were estimated for all eligible subjects from all 6 studies, the mean estimate of deaths attributable to obesity in the United States was 280184 (range, 236111-341153). Hazard ratios also were calculated from data for nonsmokers or never-smokers only. When these HRs were applied to the entire population (assuming the HR applied to all individuals), the mean estimate for obesity-attributable death was 324 940 (range, 262541-383410). CONCLUSIONS: The estimated number of annual deaths attributable to obesity among US adults is approximately 280000 based on HRs from all subjects and 325000 based on HRs from only nonsmokers and never-smokers.

Adult↗
PubMed1999

Recombinant leptin for weight loss in obese and lean adults: a randomized, controlled, dose-escalation trial.

CONTEXT: The protein hormone leptin is important to the homeostatic regulation of body weight. Treatment with exogenous leptin may affect weight loss. OBJECTIVE: To determine the relationship between increasing doses of exogenous leptin administration and weight loss in both lean and obese adults. DESIGN: A randomized, double-blind, placebo-controlled, multicenter, escalating dose cohort trial conducted from April 1997 to October 1998. SETTING: Four university nutrition and obesity clinics and 2 contract clinical research clinics. PARTICIPANTS: Fifty-four lean (body mass index, 20.0-27.5 kg/m2; mean [SD] body weight, 72.0 [9.7] kg) and 73 obese (body mass index, 27.6-36.0 kg/m2; mean [SD] body weight, 89.8 [11.4] kg) predominantly white (80%) men (n = 67) and women (n = 60) with mean (SD) age of 39 (10.3) years. INTERVENTIONS: Recombinant methionyl human leptin self-administered by daily morning subcutaneous injection (0 [placebo], 0.01, 0.03, 0.10, or 0.30 mg/kg). In part A, lean and obese subjects were treated for 4 weeks; in part B, obese subjects were treated for an additional 20 weeks. Lean subjects consumed a eucaloric diet to maintain body weight at the current value, and obese subjects were prescribed a diet that reduced their daily energy intake by 2100 kJ/d (500-kcal/d) from the amount needed to maintain a stable weight. MAIN OUTCOME MEASURES: Body weight, body fat, and incidence of adverse events. RESULTS: Weight loss from baseline increased with increasing dose of leptin among all subjects at 4 weeks (P = .02) and among obese subjects at 24 weeks (P = .01) of treatment. Mean (SD) weight changes at 4 weeks ranged from -0.4 (2.0) kg for placebo (n = 36) to -1.9 kg (1.6) kg for the 0.1 mg/kg dose (n = 29). Mean (SD) weight changes at 24 weeks ranged from -0.7 (5.4) kg for the 0.01 mg/kg dose (n = 6) to -7.1 (8.5) kg for the 0.30 mg/kg dose (n = 8). Fat mass declined from baseline as dose increased among all subjects at 4 weeks (P = .002) and among obese subjects at 24 weeks of treatment (P = .004); more than 95% of weight loss was fat loss in the 2 highest dose cohorts at 24 weeks. Baseline serum leptin concentrations were not related to weight loss at week 4 (P = .88) or at week 24 (P = .76). No clinically significant adverse effects were observed on major organ systems. Mild-to-moderate reactions at the injection site were the most commonly reported adverse effects. CONCLUSIONS: A dose-response relationship with weight and fat loss was observed with subcutaneous recombinant leptin injections in both lean and obese subjects. Based on this study, administration of exogenous leptin appears to induce weight loss in some obese subjects with elevated endogenous serum leptin concentrations. Additional research into the potential role for leptin and related hormones in the treatment of human obesity is warranted.

Adult↗
PubMed2002

Prevalence and trends in obesity among US adults, 1999-2000.

CONTEXT: The prevalence of obesity and overweight increased in the United States between 1978 and 1991. More recent reports have suggested continued increases but are based on self-reported data. OBJECTIVE: To examine trends and prevalences of overweight (body mass index [BMI] > or = 25) and obesity (BMI > or = 30), using measured height and weight data. DESIGN, SETTING, AND PARTICIPANTS: Survey of 4115 adult men and women conducted in 1999 and 2000 as part of the National Health and Nutrition Examination Survey (NHANES), a nationally representative sample of the US population. MAIN OUTCOME MEASURE: Age-adjusted prevalence of overweight, obesity, and extreme obesity compared with prior surveys, and sex-, age-, and race/ethnicity-specific estimates. RESULTS: The age-adjusted prevalence of obesity was 30.5% in 1999-2000 compared with 22.9% in NHANES III (1988-1994; P<.001). The prevalence of overweight also increased during this period from 55.9% to 64.5% (P<.001). Extreme obesity (BMI > or = 40) also increased significantly in the population, from 2.9% to 4.7% (P =.002). Although not all changes were statistically significant, increases occurred for both men and women in all age groups and for non-Hispanic whites, non-Hispanic blacks, and Mexican Americans. Racial/ethnic groups did not differ significantly in the prevalence of obesity or overweight for men. Among women, obesity and overweight prevalences were highest among non-Hispanic black women. More than half of non-Hispanic black women aged 40 years or older were obese and more than 80% were overweight. CONCLUSIONS: The increases in the prevalences of obesity and overweight previously observed continued in 1999-2000. The potential health benefits from reduction in overweight and obesity are of considerable public health importance.

Adult↗
PubMedDate not supplied

Platelet activation in obese women: role of inflammation and oxidant stress.

CONTEXT: Obesity, in particular abdominal adiposity, is associated with increased cardiovascular morbidity and mortality through mechanisms possibly linking the metabolic disorder to platelet and vascular abnormalities. OBJECTIVE: To investigate the clinical and biochemical determinants of lipid peroxidation and platelet activation in obese women. DESIGN, SETTING, AND PARTICIPANTS: Cross-sectional comparison, conducted between September 1999 and September 2001, of urinary 8-iso prostaglandin F(2alpha) (8-iso PGF(2alpha)) and 11-dehydrothromboxane B2 (11-dehyhdro-TxB2) excretion levels in 93 women: 44 with a body mass index (BMI) higher than 28 and a waist-to-hip ratio (WHR) of 0.86 or higher, android obesity; 25 with a BMI higher than 28 and a WHR lower than 0.86, gynoid obesity; and 24 nonobese women with a BMI lower than 25. An additional study was conducted to determine the short-term effects of weight loss in 20 of the 44 women with android obesity. INTERVENTION: During a 12-week period, 20 women with android obesity followed a weight loss program to reduce caloric intake to about 1200 kcal/d. MAIN OUTCOME MEASURES: Plasma C-reactive protein, insulin and leptin levels, and urinary 8-iso PGF(2alpha) (marker of in vivo lipid peroxidation) and 11-dehyhdro-TxB2 (marker of in vivo platelet activation) excretion. Weight loss was defined as successful when the initial body weight decreased by at least 5 kg after a 12-week period of caloric restriction. RESULTS: Women with android obesity had higher levels of 8-iso PGF(2alpha )(median [interquartile range [IQR]] 523 [393-685] vs 187 [140-225] pg/mg creatinine) and 11-dehyhdro-TxB2 (median [IQR], 948 [729-1296] vs 215 [184-253] pg/mg creatinine) than nonobese women (P<.001). Both 8-iso PGF(2alpha)and 11-dehyhdro-TxB2 were higher in women with android obesity than women with gynoid obesity (P<.001). Based on multiple regression analysis, C-reactive protein levels and WHRs of 0.86 or higher predicted the rate of 8-iso PGF(2alpha) excretion independently of insulin and leptin levels. Of 20 women with android obesity, 11 achieved successful weight loss, which was associated with statistically significant reductions in C-reactive protein (median change, 23%; P<.05), 8-iso PGF(2alpha) (median change, 32%; P =.04) and 11-dehydro-TxB2 (median change, 54%; P =.005). CONCLUSIONS: Android obesity is associated with enhanced lipid peroxidation and persistent platelet activation. These abnormalities are driven by inflammatory triggers related to the degree of abdominal adiposity and are, at least in part, reversible with a successful weight-loss program.

Adult↗
PubMed1999

Linkage analysis of candidate obesity genes among the Mexican-American population of Starr County, Texas.

Recent advances in the molecular basis of body fat regulation have identified several genes in which genetic variation may influence obesity and related measures in human populations. Genes that have been shown to have a regulatory function in the control of body fat utilization, eating behavior, and/or metabolic rate in rodent models of obesity include leptin (LEP), leptin receptor (LEPR), neuropeptide Y (NPY), NPY Y1 receptor (NPYY1), glucagon-like peptide-1 (GLP-1), GLP-1 receptor (GLP1R), and uncoupling protein 1 (UCP1). We have typed microsatellite markers located within or near these seven candidate obesity genes in 302 non-diabetic individuals from 59 Mexican-American families from Starr County, Texas. Sib pair linkage analysis was used to examine linkage between these genes and obesity status (obese siblings only; n = 170 pairs) and several obesity-related quantitative variables (all siblings; n = 545 total sibling pairs). Significant linkage (P = 0.042) was found between obesity and NPY within the obese sibling pairs. No other candidate gene was linked to obesity status in this subsample. Consistent with the obese sib pair linkage results, NPY showed evidence of linkage to body weight (P = 0.020), abdominal circumference (P = 0.031), hip circumference (P = 0.012), diastolic blood pressure (P = 0.005), and a composite measure of body mass and size (P = 0.048) in the entire sibling sample. Other significant linkages observed were between LEP and waist/hip ratio (P = 0.010), total cholesterol (P = 0.030), and HDL cholesterol (P = 0.026) and between LEPR and fasting blood glucose (P = 0.018) and diastolic blood pressure (P = 0.003). These results support further investigation of NPY, LEP, and LEPR to identify genetic variation that may influence obesity status, glucose and lipid metabolism, and blood pressure in Mexican Americans.

Adult↗
PubMedDate not supplied

Obesity-related complications of pregnancy vary by race.

OBJECTIVE: To evaluate racial effects on obstetric complications in obese gravidas. METHODS: The obstetric database was reviewed for the period 6/1/94 to 3/31/97. All clinic patients delivering singletons were included. Obesity was defined as a body mass index (BMI) of 29 kg/m2 or more, or a pre-pregnancy weight of 200 pounds or more. Complications studied included hypertension, diabetes, cesarean delivery, and fetal macrosomia. RESULTS: Of 2,424 eligible subjects, 168 were obese (6.9%). Obese patients had higher rates of chronic hypertension and pregestational diabetes, as well as increased rates of preeclampsia, gestational diabetes, fetal macrosomia, cesarean delivery, and operative vaginal delivery compared to nonobese patients. Of the obese patients, 105 (63%) were Hispanic, 39 (23%) were African American, and 24 (14%) were White; no Asian or Mixed/Other patients were obese. Mean BMIs of the obese subgroups did not differ (P = 0.14), but prepregnancy weights were greater in Whites than Hispanics (P < 0.002). Obese Hispanics had an increased rate of gestational diabetes (P = 0.04) and of infant weight > or =4,500 g (P =.03). Obese Hispanic and African American women were more likely than obese Whites to deliver by cesarean (P = 0.03). CONCLUSION: Racial differences affect the complication rates in obese gravidas, and may influence prenatal counseling and pregnancy management.

Adult↗
PubMed1994

A perspective on the hormonal abnormalities of obesity: are they cause or effect?

Studies in our laboratory and elsewhere have demonstrated numerous abnormalities of steroid and polypeptide hormone secretion in obesity: hyperestrogenemia and hypogonadotropic hypogonadism in obese men; diminished SHBG levels in both sexes; elevated free testosterone and free estradiol in obese women; PCOS-like gonadotropin and sex-hormone abnormalities in obese women; elevated serum insulin in both sexes; blunted stimulability of prolactin, growth hormone, and vasopressin in both sexes; and elevated basal levels and blunted stimulability and suppressibility of beta-endorphin in both sexes. All of these abnormalities have been clearly shown to be partly or completely reversible with weight loss, with the exception of the endorphin abnormalities. In that area, four out of the five studies reported show no reversibility with weight loss. Reversibility of nearly all the hormonal abnormalities of obesity (i.e., all but the hyperendorphinemia) by weight loss suggests that none of them is causative of obesity. Nevertheless, some of the reversible abnormalities may secondarily amplify the morbidity associated with obesity: the hyperinsulinemia may be related to the increased risk of hypertension, hyperlipidemia, coronary disease, and Type II diabetes; the elevated levels of free estradiol in obese women may be related to their increased risk of breast and endometrial cancer. The role of hyperendorphinemia in obesity clearly requires further investigation, since it is the only observed hormonal abnormality that appears to be non-reversible by weight loss, and also since there seems to be increased sensitivity to beta-endorphin in obesity. The possibility that endorphin abnormalities may be causal in obesity cannot be ruled out.

Adolescent↗
PubMed1998

Dealing with obesity as a chronic disease.

There are major efforts underway to educate the primary care physician about the health risks of obesity. Obesity is a chronic disease that requires chronic management. We must establish models that allow primary care physicians to participate in the chronic management of obesity, while recognizing that the interest and ability of primary care physicians to participate in obesity management will vary. Three general models of obesity management are proposed for the primary care physician, ranging from minimal evaluation to complete evaluation and treatment. In order for the models to be implemented, we must consider establishing a category of obesity specialists who can develop comprehensive treatment programs to which patients with obesity can be referred, and who can provide leadership and guidance for primary care physicians who are involved in obesity management. The North American Association for the Study of Obesity (NAASO) could help establish obesity specialists and provide a structure to allow them to provide leadership for obesity treatment.

Chronic Disease↗
PubMed1995

Augmented production of tumor necrosis factor-alpha in obese mice.

Non-insulin-dependent diabetes mellitus develops in obesity. The insulin resistance of this disease may be mediated by tumor necrosis factor-alpha (TNF-alpha). In particular, the TNF-alpha derived from adipose tissues might be involved in the induction of peripheral insulin resistance in rodent models of obesity. In general, monocytes/macrophages have been considered as the major source of TNF-alpha. This study was designed to examine the potential production of TNF-alpha from monocyte/macrophages in obese mice. In obese (ob/ob) and obese diabetic (db/db) mice, both of which are known to have severe insulin resistance, unstimulated serum bioactivity of TNF-alpha was significantly higher than that in lean control mice. Spontaneous TNF-alpha mRNA expression in splenic macrophages was also enhanced in obese mice, but not in monosodium-L-glutamate (MST)-induced obese mice which have no insulin resistance. In addition, both ob/ob and db/db mice produce more TNF-alpha than lean mice upon in vivo lipopolysaccharide (LPS) stimulation. The LPS-induced increase in serum TNF-alpha activity was not observed in MSG-induced obese mice. Taken together, it is postulated that TNF-alpha produced by monocytes/macrophages may also play an important role in the genesis of insulin resistance in obesity. Further study is needed to reveal the mechanism of enhanced TNF-alpha production in obese states and its possible etiologic relevance to obesity.

Animals↗
PubMed2000

Does breast-feeding protect against childhood obesity?

The impact of breast-feeding on overweight and obesity in children at school entry was assessed in a cross sectional study in Bavaria in 1997. The school entry health examination enrolled 134,577 children. Data on early feeding were collected in two rural districts (eligible population n=13,345). The analyses were confined to 5 or 6 year old children with German nationality. The main outcome measures were overweight (BMI>90th percentile for all German children seen at the 1997 school entry health examination in Bavaria) and obesity (BMI>97th percentile). Information on breast-feeding was available for 9206 children of whom 56% had been breast-fed for any length of time. In non breast-fed children the upper tail of the BMI distribution was enlarged as compared to the breast-fed children whereas the median was almost identical. The prevalence of obesity in children who had never been breast-fed was 4.5% as compared to 2.8% in ever breast-fed children. A clear dose response effect for the duration of breast-feeding on the prevalence of obesity was found: 3.8%, 2.3%, 1.7% and 0.8% for exclusive breast-feeding for up to 2, 3 to 5, 6 to 12 and more than 12 months, respectively. The results for overweight were very similar. The protective effect of beast feeding on overweight and obesity could not be explained by differences in social class or lifestyle. The adjusted odds ratios of breast-feeding for any length of time was 0.71 (95% CI 0.56-0.90) for obesity and 0.77 (95%CI 0.66-0.88) for overweight. This data set did not allow to adjust for maternal weight, an important risk factor for obesity in children. Maternal overweight, however, could not explain the effect of breastfeeding on overweight and obesity in a similar study. The reduction in the risk for overweight and obesity is therefore more likely to be related to the properties of human milk than to factors associated with breast-feeding. The potential relevance of different components of human milk for the observed reduction in the risk for overweight and obesity is discussed. The preventive effect of breast-feeding on overweight and obesity is an important additional argument for the promotion of breast-feeding in industrialised countries.

Body Mass Index↗
PubMed1994

Catecholamine resistance in fat cells of women with upper-body obesity due to decreased expression of beta 2-adrenoceptors.

Upper-body obesity is an important risk factor for developing non-insulin dependent diabetes. To investigate the possibility that a lipolysis defect is present in this form of obesity, we examined the adrenergic regulation of lipolysis in abdominal subcutaneous fat cells from 25 women with upper-body obesity and 24 non-obese women. Lipolytic noradrenaline sensitivity (but not the maximum rate of lipolysis) was reduced by 10-fold in obese women (p < 0.01). The noradrenaline resistance could be ascribed to a 10-fold decrease in lipolytic beta 2-adrenoceptor sensitivity (p < 0.01). The lipolytic sensitivity of beta 1- and alpha 2-adrenergic receptors was normal in the obese women. A 70% reduction in the cell surface density of beta 2-adrenoceptors was observed compared to the control subjects (p < 0.01). However, beta 1-receptor density as well as steady-state mRNA levels for beta 1- and beta 2-receptors were normal in obese women. Lipolytic noradrenaline sensitivity correlated inversely with BMI (adjusted r2 = 0.76 together with fat cell volume in stepwise regression analysis). The fasting plasma level of free cortisol was 30% lower in obese compared to non-obese women (p < 0.05) but obesity did not influence resting plasma catecholamine levels. Thus, lipolytic catecholamine resistance is present in abdominal obesity, due to low density of beta 2-adrenoceptors, which in its turn may be caused by a post-transcriptional defect in beta 2-receptor expression.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗
PubMed1987

Differences in ventilatory responses to hypoxia and hypercapnia between normal and judo athletes with moderate obesity.

Hypercapnic and hypoxic ventilatory sensitivities were compared in twenty-one judoists and 24 control subjects with similar degrees of moderate obesity. Data from ten non-obese control subjects were also included as a reference. Mean body weight (BW) and % of ideal body weight in the judoists and the obese and non-obese controls were 100 +/- 14.8, 94.4 +/- 5.3 and 63.4 +/- 6.1 (mean +/- SD) kg, and 142.3 +/- 16.7, 142.2 +/- 12.9 and 98.4 +/- 10.7%, respectively. Mean body fat in the judoists was 16.2 +/- 13.9%, being 25.3 +/- 7.7% in the obese control group, the difference being significant (p less than 0.01). Hypercapnic sensitivities in terms of the CO2 ventilatory response slope (S) and its normalized value for 70 kg BW (SN) of the obese controls were higher than the judoists. These findings were also verified by the CO2-occlusion pressure responses. S and SN in the obese controls were significantly correlated with BW and % body fat. However, no positive correlation was found between BW and S or SN in the judoists as well as between lean body mass and S or SN in the obese control. Hypoxic sensitivity in terms of the PETO2-ventilation hyperbola slope (A) and its normalized value (AN) in the obese control was significantly higher than the non-obese control, but the difference from the judoists was not significant. A and AN were found to increase with increasing % body fat in both judoists and obese controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗
PubMed1987

Gastric secretion in massive obesity. Evidence for abnormal response to vagal stimulation.

Studies in animals and man suggest involvement of the vagal nerve in the pathophysiology of massive obesity. An abnormal vagal response pattern has been found in the obese rat, but corresponding functional studies in obese man are nonexistent. The gastric acid secretion was therefore examined in 13 nondiabetic grossly obese patients (average body weight 120 kg) and compared to 16 age-matched controls of normal body weight. The gastric acid response to modified sham feeding was significantly (P less than 0.05) reduced in obese patients, being on average 60% of the control output. The obese patients had a higher maximal gastric acid response to graded intravenous pentagastrin, 36.6 +/- 2.9 mmol/hr, compared to 27.1 +/- 2.4 mmol/hr in controls (P less than 0.05). In addition, the patients seemed to need less pentagastrin to reach a secretory plateau. Basal acid secretion rates were similar in obese and control groups. Plasma gastrin and blood glucose were not significantly different in obese patients and controls, but patients had significantly elevated plasma insulin levels. The change of plasma insulin during the sham-feeding procedure correlated with the magnitude of the secretory response in obese and control subjects. The reduced gastric acid response to vagal stimulation in the absence of impaired parietal cell function in obese patients is indicative of an association between massive obesity and altered vagal function in man.

Blood Glucose↗