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Insulin secretion in the obese (ob/ob) mouse. The effect of oxytetracycline on insulin release.

The effect of oxytetracycline (OTC) pretreatment on the response of the ob/ob mouse to insulin secretagogues in vivo and in vitro was investigated. With glucose loading in vivo, the peak glucose was twofold greater and the insulin levels threefold greater in obese than in lean mice. After OTC treatment, there was no significant difference an insulin levels between lean and obese mice although the peak glucose level was still obese mice although the peak glucose level was still 1.5 times as high. Glucagon increased plasma glucose 2.5-fold and plasma insulin 20-fold in the obese as compared with lean mice. After OTC treatment the glycemic response of the obese was indistinguishable from that of the lean control. The insulin levels, while higher than those of lean mice, were only 25% of those found in the untreated obese. Aminophylline produced an 8- and a 20-fold increase in peak glucose and insulin levels, respectively, as compared with lean mice. In the OTC-treated obese mice, the injection of aminophylline produced a slower rise in plasma glucose than in the obese controls, but the levels were not significantly different from those of the untreated obese mice at 90 min. On the other hand, the insulin levels attained a plateau at a value which was one-fifth that found in the control obese group. In vitro, isolated islets from obese mice showed an exaggerated response to the secretagogues. Pretreatment with OTC attenuated this response. The fraction of insulin released at 10 mM glucose was less than one-fourth that in the obese controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminophylline↗

Gastric inhibitory polypeptide (GIP) and insulin release in the obese Zucker rat.

The involvement of the gut hormone GIP (gastric inhibitory polypeptide, glucose-dependent insulinotropic polypeptide) in the hyperinsulinemia of the adult obese Zucker rat was investigated. Glucose, insulin, and GIP responses to oral glucose were compared in lean and obese rats. The sensitivity of the isolated, perfused pancreas to glucose and GIP was studied in basal and hyperglycemic conditions in lean and obese rats. Immunocytochemical studies of the gut and pancreas were also carried out. The glucose and GIP responses to oral glucose were similar in lean and obese rats, but obese animals were hyperinsulinemic compared with lean controls under fasting conditions and after oral glucose. The isolated, perfused pancreas of obese Zucker rats had an elevated insulin response to 300 mg/dl glucose. GIP increased the insulin response to 300 mg/dl glucose threefold in both lean and obese rats. At basal glucose levels (80 mg/dl), GIP augmented insulin release in obese but not in lean rats. Immunocytochemical studies demonstrated the presence of enlarged islets in obese rats due to an increase in the B-cell mass. A-, D-, and PP-cells appeared normal. Obese and lean rats had similar numbers of GIP-containing cells in the gut. This study suggests that GIP may contribute to the fasting hyperinsulinemia characteristic of adult obese Zucker rats. GIP infusion to achieve levels equivalent to those seen in the basal state are capable of stimulating insulin release in the absence of hyperglycemia in the obese rat, which suggests an impairment of the regulatory mechanisms controlling the glucose-dependent insulinotropic action of GIP in these animals.

Animals↗

Postprandial free fatty acid kinetics are abnormal in upper body obesity.

Excess free fatty acid release (rate of appearance) is seen in overnight postabsorptive, upper body obese women and, if present postprandially, could contribute to glucose intolerance. These studies examine the antilipolytic effect of a mixed meal in upper body obese, lower body obese, and nonobese women and the contribution of meal triglyceride fatty acids to circulating free fatty acids. Eight upper body obese, 8 lower body obese, and 8 nonobese age-matched, premenopausal women were studied. Systemic oleate Ra ([3H]oleate) was measured before and after an evening meal that contained triolein labeled with [14C]triolein as the only source of fat. Premeal oleate Ra was greater in both upper body obese and lower body obese women than nonobese women. The nadir of total oleate Ra occurred 90-240 min postprandially and was less (P < 0.01) in nonobese and lower body obese women (63 +/- 10 and 87 +/- 17 mumol/min) than in upper body obese women (140 +/- 21 mumol/min). Meal oleate Ra contributed substantially to total oleate Ra. The nadir for endogenous oleate Ra in nonobese and lower body obese women was less (P < 0.01) than that observed in upper body obese women. We conclude that the antilipolytic effect of a mixed meal is reduced in upper body obese women and that meal triglyceride fatty acids contribute significantly to postprandial free fatty acid flux.

Adult↗

Contribution of obesity to defects of intracellular glucose metabolism in NIDDM.

OBJECTIVE: To examine the contribution of obesity to insulin resistance and abnormalities of intracellular glucose and fat metabolism in NIDDM. RESEARCH DESIGN AND METHODS: Glucose turnover measurements and indirect calorimetry were performed in 10 obese non-insulin-dependent diabetes mellitus (NIDDM) and 10 lean NIDDM subjects (body mass index 35.3 +/- 1.0 vs. 24.1 +/- 0.5 kg/m2, P < or = 0.001) in the basal state and during hyperinsulinemic (720 pmol.m-2.min-1) euglycemic (5.0-5.5 mmol/l) clamps. RESULTS: Obese and lean NIDDM subjects demonstrated similar basal rates of glucose uptake (GU) (1.15 +/- 0.08 vs. 1.26 +/- 0.08 mmol/min, NS) as well as oxidative (0.49 +/- 0.07 vs. 0.53 +/- 0.05 mmol/min, NS) and nonoxidative (0.67 +/- 0.10 vs. 0.73 +/- 0.12 mmol/min, NS) glucose metabolism. During hyperinsulinemic glucose clamp studies, rates of GU were lower in obese NIDDM subjects (34.1 +/- 2.3 vs. 55.2 +/- 3.8 mumol.kg fat-free mass [FFM]-1.min-1, P < or = 0.001) as were rates of oxidative (14.1 +/- 1.3 vs. 22.1 +/- 2.1 mumol.kg FFM-1.min-1, P < or = 0.005) and nonoxidative (20.0 +/- 2.3 vs. 33.1 +/- 3.6 mumol.kg FFM-1. min-1, P < or = 0.01) glucose metabolism. Although absolute rates of insulin-stimulated GU were decreased in the obese group, the relative distribution into glucose oxidation (GOX) and nonoxidative glucose metabolism (NOX) was comparable in both groups (GOX 42% in obese and 41% in lean subjects; NOX 58% in obese and 59% in lean subjects). The NIDDM groups had similar basal free fatty acid levels that were suppressed equally during hyperinsulinemic clamps. However, basal fat oxidation (Fox) was greater in the obese NIDDM group (103 +/- 11 vs. 73 +/- 8 mumol/min, P < or = 0.05) and was less suppressed to insulin (74 +/- 13 vs. 16 +/- 3 mumol/min, P < or = 0.001). CONCLUSIONS: These results indicate that when obesity is present in NIDDM subjects with this degree of hyperglycemia, insulin-stimulated GU is lower by 35-40%. Reduced GU in obese NIDDM subjects leads to decreased intracellular substrate availability and lower rates of oxidative and nonoxidative glucose metabolism. Insulin suppression of Fox is also impaired when obesity is present and may contribute to decreased insulin-mediated GU in NIDDM. We conclude that obesity increases insulin resistance in NIDDM primarily by effects on GU rather than the intracellular pathways of glucose metabolism.

Adipose Tissue↗

Effect of weight loss on resting energy expenditure in hypertensive and normotensive obese women.

Hyperinsulinemia and the associated increased sympathetic nervous activity have been proposed to implicate in the development of hypertension and obesity. The role of hyperinsulinemia in mediated resting energy expenditure (REE) in hypertensive obese subjects is not clear. The effect of weight loss on REE between hypertensive and normotensive obese women are also unknown. We measured fasting plasma glucose, insulin, lipids concentrations, REE and body composition by bioelectrical impedance methods before and after a weight loss program in 9 newly diagnosed hypertensive and 10 normotensive obese women. As compared with age-matched lean control women (n=14), obese subjects had higher fasting plasma glucose, insulin concentrations and REE values. However, these variables were not different between obese groups. Although REE and fasting plasma insulin concentrations correlated well in simple correlation (r=0.708, p<0.001), this relationship disappeared after adjusting for values of fat free mass (FFM). Weight loss for approximately 10% of initial weight led to significant decreases of blood pressure and fasting plasma insulin concentrations in both obese groups. Fasting plasma cholesterol, LDL cholesterol and triglyceride concentrations decreased in hypertensive obese individuals. Significant fall of REE in hypertensive group (p<0.05) and normotensive group (p<0.02) were observed following weight loss. However, the ratio of REE to FFM decreased significantly only in hypertensive subjects (114.6+/-5.2 KJ/day x Kg(-1) to 107.2+/-4.6 KJ/day x Kg(-1), p<0.05). In conclusion, obese women, either hypertensive or normotensive, had higher fasting plasma insulin concentrations and REE than those of lean controls, although these variables were not different between obese groups. No significant relation between fasting plasma insulin and REE could be found. Weight loss produced a significant decrease of REE/FFM only in hypertensive obese women. Further study to evaluate the effect of weight loss on energy expenditure in hypertensive obese subjects is necessary.

Adult↗

Dietary fat type and level influence adiposity development in obese but not lean Zucker rats.

The development of obesity is influenced by a variety of factors including genetics and dietary fat type and level. To examine the interaction between these factors, male lean and obese Zucker rats (5 weeks initial age) were fed either a low-fat (15% calories) or one of two high-fat diets (65% calories; predominant fat source of either soybean oil or palm olein) for 8 weeks. Body weight, food intake, indirect calorimetry, and body composition determinations were performed. As expected, food intake, body weight, feed efficiency, oxygen consumption, heat production and carcass lipid were all significantly higher in obese compared to lean rats. Dietary fat level and/or type influenced body weight gain, oxygen consumption, heat production, energy balance, and carcass weight and lipid content in the obese but not in the lean Zucker rats. Oxygen consumption and carcass weight were increased approximately 25% and 10% respectively in obese rats fed either of the two high-fat diets as compared to those fed the low-fat diet. The type of fat fed in the high-fat diets also influenced body weight gain, heat production, energy balance, and carcass lipid content of the obese rats. Body weight gain and carcass lipid content were increased (16%-17%; P < 0.005) in obese rats fed the high-fat palm olein diet as compared to those fed the low-fat diet. These parameters were not increased in obese rats fed the high-fat soybean oil diet. In contrast, indirect calorimetry measurements indicated a moderate increase in heat production (Kcal/effective body mass/day; 14.5%) and decrease in energy balance (44.8%) in the obese rats fed the high-fat soybean oil diet as compared to those fed the low-fat diet. Energy expenditure and lipid accumulation were negligibly influenced by dietary fat level or type in the lean Zucker rats. The differential response of the lean and obese Zucker rats to this short-term dietary manipulation demonstrate that genetic background can influence an individual's response to dietary fat type and level. The genetically obese Zucker rat appears to be a good model for further studies of high-fat diet-induced obesity.

Adipose Tissue↗

The costs of obesity among full-time employees.

PURPOSE: To quantify annual costs attributable to obesity, including both increased medical expenditures and absenteeism, separately for overweight and three categories of obesity (i.e., obesity grades I, II, and III) among men and women with full-time employment. DESIGN: Standard econometric methods were used to separately estimate overweight and obesity-attributable medical expenditures and absenteeism. SETTING: The civilian noninstitutionalized population of the United States. SAMPLE: Two nationally representative and publicly available datasets (with response rates of at least 60%) were restricted to participants 18 to 64 years old and employed full-time for the entire year. The final datasets used to estimate obesity-attributable medical expenditures and absenteeism included 20,329 and 25,427 adults, respectively. MEASURES. Annual medical expenditures and missed work days due to illness or injury. ANALYSIS RESULTS: Overweight and obesity-attributable costs range from dollar 175 per year for overweight male employees to dollar 2485 per year for grade-II obese female employees. The costs of obesity (excluding overweight) at a firm with 1000 employees are estimated to be dollar 285,000 per year CONCLUSIONS: Obesity results in significant increases in medical expenditures and absenteeism among full-time employees. Approximately 30% of the total costs result from increased absenteeism, and although those with grade-III obesity represent only 3% of the employed population, they account for 21% of the costs due to obesity. These estimates do not consider other potential costs associated with obesity, including disability and presenteeism.

Adult↗

Incidence of obesity in parturients scheduled for caesarean section, intra-operative complications, management and outcome.

OBJECTIVES: To determine the incidence of obesity in parturients scheduled for Caesarean section, identify intra-operative complications, management and outcome. DESIGN: A prospective observational study. SETTING: University of Benin Teaching Hospital, a university-affiliated tertiary centre. SUBJECTS: Parturients scheduled for Caesarean section excluding patients in American Society of Anaesthesiologists (ASA) health status 4 and 5. RESULTS: Three hundred patients were recruited in the study. One hundred and forty eight (49.3%) were non-obese (BMI < 30kgm2) while 152 (50.7%) were obese (BMI >30kgm(-2)). The incidence of obesity was extremely significant P<0.0001, t = 19.721 and 95% C.I. = 11.998 - -9.820. Twenty four percent of the obese and 6% of the non-obese parturients had intercurrent medical diseases. 40.5% of the non-obese parturients had general anaesthesia while 13.1% of the obese parturients were offered general anaesthesia. The incidence of intra-operative complications was higher in the obese group. P<0.0001; extremely significant. Odds ratio = 3.647; 95% C.I. of 2.0007 - 6.626. The most common complications were hypotension (n = 14), shivering (n = 12) and inadequate anaesthesia (n = 8). CONCLUSION: There is a high incidence of obesity in parturients. This group of patients constitutes a high risk group in obstetric anaesthesia. The incidence of complications was higher in the obese than in the non-obese.

Adult↗

The natural history of the development of obesity in a cohort of young U.S. adults between 1981 and 1998.

BACKGROUND: Understanding the natural history of obesity in a population may be a critical step toward developing effective interventions. OBJECTIVE: To assess the development of body mass and examine the role of race or ethnicity, sex, and birth year in obesity onset in young U.S. adults. DESIGN: Prospective cohort study. SETTING: The National Longitudinal Survey of Youth 1979, a national sample with oversampling of minority ethnic groups. PARTICIPANTS: 9179 persons. MEASUREMENTS: Body mass index (BMI) calculated from 12 self-reported height and weight samples recorded between 1981 and 1998. Logistic regression identified predictors of obesity at age 35 to 37 years. Cox proportional hazards models compared the incidence of obesity by ethnicity and birth year. RESULTS: Overall, 26% of men and 28% of women were obese (BMI > or = 30 kg/m2) by age 35 to 37 years. Race or ethnicity and baseline BMI were significant predictors of obesity. Obesity onset was 2.1 (95% CI, 1.6 to 2.7) times faster for black women and 1.5 (CI, 1.1 to 2.0) times faster for Hispanic women than for white women. The pattern for men differed: Overall, obesity developed most rapidly in Hispanic men, but relative rates of obesity onset for white men compared with black men varied according to age. The rate of obesity onset increased 26% to 28% over an 8-year span in birth year. CONCLUSIONS: Marked ethnic-based differences were found in rates of weight accumulation in young U.S. adults, with later birth cohorts experiencing earlier onset of obesity. To alter the course of obesity in the United States, interventions should target young adults, especially those of minority ethnic groups.

Adult↗

Obesity in adulthood and its consequences for life expectancy: a life-table analysis.

BACKGROUND: Overweight and obesity in adulthood are linked to an increased risk for death and disease. Their potential effect on life expectancy and premature death has not yet been described. OBJECTIVE: To analyze reductions in life expectancy and increases in premature death associated with overweight and obesity at 40 years of age. DESIGN: Prospective cohort study. SETTING: The Framingham Heart Study with follow-up from 1948 to 1990. PARTICIPANTS: 3457 Framingham Heart Study participants who were 30 to 49 years of age at baseline. MEASUREMENTS: Mortality rates specific for age and body mass index group (normal weight, overweight, or obese at baseline) were derived within sex and smoking status strata. Life expectancy and the probability of death before 70 years of age were analyzed by using life tables. RESULTS: Large decreases in life expectancy were associated with overweight and obesity. Forty-year-old female nonsmokers lost 3.3 years and 40-year-old male nonsmokers lost 3.1 years of life expectancy because of overweight. Forty-year-old female nonsmokers lost 7.1 years and 40-year-old male nonsmokers lost 5.8 years because of obesity. Obese female smokers lost 7.2 years and obese male smokers lost 6.7 years of life expectancy compared with normal-weight smokers. Obese female smokers lost 13.3 years and obese male smokers lost 13.7 years compared with normal-weight nonsmokers. Body mass index at ages 30 to 49 years predicted mortality after ages 50 to 69 years, even after adjustment for body mass index at age 50 to 69 years. CONCLUSIONS: Obesity and overweight in adulthood are associated with large decreases in life expectancy and increases in early mortality. These decreases are similar to those seen with smoking. Obesity in adulthood is a powerful predictor of death at older ages. Because of the increasing prevalence of obesity, more efficient prevention and treatment should become high priorities in public health.

Adult↗

Effects of obesity on the cytochrome P450 enzyme system.

OBJECTIVE: This review evaluates the effect of obesity on the various isozymes of the cytochrome P450 enzyme system. MATERIALS AND METHOD: A Medline search of the international literature on drug metabolism and obesity from 1966 to early 1998 was conducted. All English language studies in humans that compared the pharmacokinetics of a given medication between obese and non-obese subjects were evaluated. Any study in which the substrate examined is excreted unchanged, not metabolized primarily by a single cytochrome P450 isozyme or which is considered a high extraction compound was excluded from this review. RESULTS: Despite the prevalence of obesity, the known health consequences of obesity and the increase of medication usage in the obese population, very few studies have attempted to establish the effect of this condition on the cytochrome P450 enzyme system. Numerous studies, however, have compared pharmacokinetic parameters between obese and non-obese subjects for individual drugs. By examining those trials in which the agents studied all undergo biotransformation via the same CYP450 isozyme, a preliminary appreciation of the effect of obesity on the activity of that particular isozyme can be attained. CONCLUSIONS: The effect of obesity on CYP450 appears to be isozyme-specific with the activity of cytochrome P450 3A4 decreasing and that of cytochrome P450 2E1 increasing. The effect of obesity on the cytochrome P450 1A2, 2C9, 2C19, and 2D6 isozymes is inconclusive.

Cytochrome P-450 Enzyme System↗

The cost of obesity in Canada.

BACKGROUND: Almost one-third of adult Canadians are at increased risk of disability, disease and premature death because of being obese. In order to allocate limited health care resources rationally, it is necessary to elucidate the economic burden of obesity. OBJECTIVE: To estimate the direct costs related to the treatment of and research into obesity in Canada in 1997. METHODS: The prevalence of obesity (body mass index of 27 or greater) in Canada was determined using data from the National Population Health Survey, 1994-1995. Ten comorbidities of obesity were identified from the medical literature. A population attributable fraction (PAF) was calculated for each comorbidity with data from large cohort studies to determine the extent to which each comorbidity and its management costs were attributable to obesity. The direct cost of each comorbidity was determined using data from the Canadian Institute of Health Information (for direct expenditure categories) and from Health Canada (for the proportion of expenditure category attributable to the comorbidity). This prevalence-based approach identified the direct costs of hospital care, physician services, services of other health professionals, drugs, other health care and health research. For each comorbidity, the cost attributable to obesity was determined by multiplying the PAF by the total direct cost of the comorbidity. The overall impact of obesity was estimated as the sum of the PAF-weighted costs of treating the comorbidities. A sensitivity analysis was completed on both the estimated costs and the PAFs. RESULTS: The total direct cost of obesity in Canada in 1997 was estimated to be over $1.8 billion. This corresponded to 2.4% of the total health care expenditures for all diseases in Canada in 1997. The sensitivity analysis revealed that the total cost could be as high as $3.5 billion or as low as $829.4 million; this corresponded to 4.6% and 1.1% respectively of the total health care expenditures in 1997. When the contributions of the comorbidities to the total cost were considered, the 3 largest contributors were hypertension ($656.6 million), type 2 diabetes mellitus ($423.2 million) and coronary artery disease ($346.0 million). INTERPRETATION: A considerable proportion of health care dollars is devoted to the treatment and management of obesity-related comorbidities in Canada. Further research into the therapeutic benefits and cost-effectiveness of management strategies for obesity is required. It is anticipated that the prevention and treatment of obesity will have major positive effects on the overall cost of health care.

Adult↗

Role of genetic factors in childhood obesity and in susceptibility to dietary variations.

The concern about the current epidemic of obesity is heightened by recent data showing an increase in the prevalence of overweight and obesity in children and adolescents. As obese children are at increased risk of becoming obese adults, early identification of individuals at risk of becoming obese is important for the implementation of preventive measures. In that context, it is important to assess the role of genetic and nongenetic factors in childhood obesity as well as in susceptibility to dietary variations. This paper reviews recent data regarding the prevalence of obesity in childhood as well as the role of genetic factors in phenotypes related to obesity, with emphasis on studies conducted on children, when available. The existence of severe cases of obesity, such as those encountered in Mendelian syndromes of obesity or those caused by mutations in single genes, provides strong evidence for a role of genetic factors in the aetiology of childhood obesity. Furthermore, results from family studies suggest that the maximal heritability of obesity phenotypes ranges from about 30% to 50% and that the major affectors of body fat content, energy intake and energy expenditure are also influenced by genetic factors. Finally, there is increasing evidence that responsiveness to dietary intervention is genetically determined.

Adolescent↗

Diabetes and obesity in the Louisiana Coushatta Indians.

OBJECTIVE: In order to assist their community in planning intervention and prevention programs, prevalence rates for diabetes and obesity were examined among the Louisiana Coushatta. RESEARCH DESIGN AND METHODS: Coushatta individuals participated in a health survey (questionnaires and physical examinations). Those without known diabetes underwent oral glucose tolerance testing and were classified as having normal glucose tolerance (NGT), impaired glucose tolerance (IGT), or diabetes mellitus (DM). Those with known DM had the diagnosis confirmed by history and/or elevated hemoglobin A1c. Waist-to-hip ratio (WHR), body mass index (BMI), and percent body fat (%BF) were determined as measures of central adiposity and obesity. Prevalence rates of diabetes and obesity among those examined were calculated. The prevalence of those with more than one anthropometric index positive for obesity was also determined. RESULTS: The prevalence of DM was 30% and IGT was 17% among the first 151 Coushatta participants. For males, the prevalence of obesity was 62%, 57%, and 52%, and for females, 59%, 54%, 45%, as determined by the BMI, %BF, and WHR, respectively. Obesity was more prevalent among those with glucose intolerance (IGT + DM) than those with NGT, and those who were obese had the highest prevalence of glucose intolerance. A greater percentage of those with glucose intolerance had more than one positive obesity measure as compared to those with NGT, and those with more than one index consistent with obesity had a greater prevalence of IGT + DM. CONCLUSIONS: Prevalence rates of DM and obesity are high among the Louisiana Coushatta, and obesity is associated with glucose intolerance. Clustering of the three obesity measures occurs in a high percentage of individuals. Data from the current survey are providing information that is being used by the Coushatta community for health planning and development of intervention and prevention programs.

Adolescent↗

Lateral hypothalamic serotonergic responsiveness to food intake in rat obesity as measured by microdialysis.

The hypothalamic serotonergic system is involved in the regulation of food ingestion and energy metabolism. Since disturbances of both energy intake and expenditure can contribute to obesity, the objective of the present study was to evaluate the serotonergic response stimulated by food ingestion in two different models of obesity: the hyperphagic Zucker and the hypophagic and hypometabolic, monosodium glutamate (MSG) obese Wistar rat. For this we used microdialysis to examine the release of 5-hydroxytryptamine (serotonin, 5HT) and 5-hydroxyindoleacetic acid (5HIAA) in the lateral hypothalamus. Daily intake of MSG-obese rats was 40% lower while that of Zucker obese rats was 60% higher than that of the respective lean controls. In overnight-fasted animals, 20-min microdialysate samples were collected before (basal release) and during a 2-h period of access to a balanced palatable food mash. The animals began to eat during the first 20 min of food access, and food consumption was similar among the four groups in all six individual 20-min periods recorded. Ingestion of food increased 5HT release in all groups. In MSG-obese and lean Wistar rats, 5HT levels were similarly elevated during the whole experimental period. In the Zucker strain, 5HT increments of basal release tended to be higher in obese than in lean rats at 20 and 40 min, and a significantly higher increment was observed at 60 min after food access (40 and 135% for lean and obese, respectively). The area under the curve relating serotonin levels to the 120 min of food availability was significantly higher in Zucker obese (246.7 +/- 23.3) than MSG-obese (152.7 +/- 13.4), lean Wistar (151.9 +/- 11.1), and lean Zucker (173.5 +/- 24.0) rats. The present observation, of a food-induced serotonin release in the lateral hypothalamus of lean Wistar and Zucker rats, evidences that 5HT in the lateral hypothalamus is important in the normal response to feeding. In obese animals, the serotonin response was similar to (in the hypophagic-hypometabolic MSG model) or even higher than (in the hyperphagic Zucker model) that seen in the respective lean controls. This result indicates that the energy homeostasis disturbances of both these obesity models may not be ascribed to an impairment of the acute lateral hypothalamic serotonin response to a dietary stimulus.

Animals↗

[Investigation and comparison of the beta(3)-adrenergic receptor gene Trp64Arg mutation in simple obesity and metabolic syndrome].

OBJECTIVE: To investigate and compare Trp64Arg mutation of beta(3)-adrenergic receptor (beta(3)-AR) gene in simple obesity and metabolic syndrome (MS), and to correlate the mutation difference with sex, total body fat and fat distribution. METHODS: Mutation study was carried out with PCR in 295 subjects with simple obesity and 219 subjects with MS. The subjects were stratified by body mass index (BMI) as light obesity group (BMI 25 approximately 29.9 kg/m(2)) and serious obesity group (BMI >/= 30 kg/m(2)) and by mean of waist circumference (WC) as abdominal adipose tissue light depot group (WC < 104 cm in male and WC < 88 cm in female) and serious depot group (WC >/= 104 cm in male and WC >/= 88 cm in female). 175 healthy non-obese subjects were selected as controls. RESULTS: The frequency of Trp64Arg mutation of beta(3)-AR gene was higher in the male subjects with MS than those with simple obesity and non-obese controls (32.25%, 21.01% and 19.91%, respectively, P < 0.05) and also higher than female ones with MS (32.35% vs 23.46%, P < 0.01). It was found by further stratification that the frequency of Trp64Arg mutation of beta(3)-AR gene was higher in the male light obesity group with MS than female light obesity group with MS. The frequency is also higher than that in the male light obesity group of the obese subjects (32.83% vs 17.35%, P < 0.05 and 32.83% vs 20.41%, P < 0.05, respectively). The frequency of mutation was higher in male abdominal adipose tissue serious depot subjects with MS than those with simple obesity (35.71% vs 20.16%, P < 0.05). CONCLUSION: Trp64Arg mutation of beta(3)-AR gene may be used as a genetic marker for MS in male.

Adult↗

The prevalence of childhood obesity in primary school children in urban Khon Kaen, northeast Thailand.

Childhood obesity is a serious public health problem because of its strong association with adulthood obesity and the related adverse health consequences. The published literature indicates a rising prevalence of childhood obesity in both developed and developing countries. However no data exists on the prevalence in Northeast Thailand, one of the poorest regions of the country and one that has experienced a recent economic transition. The objective of this study was to estimate the prevalence of obesity in seven to nine year old children in urban Khon Kaen, Northeast Thailand. A cross-sectional school based survey was conducted to determine the prevalence of obesity in children of urban Khon Kaen, Thailand. Multi-staged cluster sampling was used to select 12 school clusters of 72 children each between the ages of 7 and 9 years, in primary school grades 1, 2 and 3 from government, private and demonstration schools. A total of 864 seven to nine year old school children were studied. Anthropometric measurements of standing height and weight were taken for all subjects to the nearest tenth of a centimetre and tenth of a kilogram respectively, Childhood obesity was defined as a weight-for-height Z-score above 2.0 standard deviations of the National Center for Health Statistics/World Health Organisation reference population median. The prevalence of childhood obesity was 10.8% (95% CI: 7.6, 13.9). Obesity was significantly more prevalent in boys than girls. The biggest difference was observed between the three school types, with the highest prevalence of obesity found at teacher training demonstration schools and the lowest at the government schools. This study provides the first data on childhood obesity prevalence in Northeast Thailand. The prevalence of 10.8 per cent is lower than that found in two other urban areas of Thailand but slightly higher than expected for this relatively poor region. If this prevalence rate increases, as observed in other countries in economic transition, the incidence of non-communicable diseases associated with obesity is also likely to increase, thus raising cause for concern and reason for intervention to both control and prevent obesity during childhood.

Body Height↗

A perspective on obesity.

This article represents another approach to the topic of obesity in African-American women. It will not give the usual statistical data on obesity in African American women, because as African-American women, it is known that a greater majority is at risk. Instead the article represents a historical, cultural and psychosocial journey in attempting to understand obesity in African-American women from this perspective. The following thoughts are reflective of interactions with African-American women who have struggled with their weight and who have strived to understand the dynamics of their dilemma of being overweight and/or obese in America. This article explains that obesity in African-American women is more than an alteration in ones physiological processes. For some African-American women obesity is the essence of ones being and it has had a deleterious impact on them. Obesity in the African-American woman is not as simplistic as perceived. It is more than the management of the intake of food. Obesity is also more than the type of food that African-American women prepare and consume. Obesity in this sense maybe linked to the very essence of the women's cultural, historical and psychosocial well being. Being large can be a familial characteristic bearing no connection to the consumption and preparation of food. Important to the latter concept, and essential to the understanding of obesity in African-American women, it needs to be remembered that food may have many symbolic meanings. The symbols may be of a cultural and psychological nature and could be consciously unknown to the individual. Whatever the situation, it needs to be clear that for many African-Americans, obesity is not merely a medical problem. Being obese in America, and particularly for African-American women, has a far-reaching effect. It has reek havoc on the cultural psyche of the African-American women. The popular cultural concept conveyed by all types of media, is one of being thin and/or slim.

Black or African American↗