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PubMed1986

Adrenalectomy induced anorexia in gold thioglucose-treated obese mice: metabolic and hormonal changes.

Adrenalectomy of gold thioglucose (GTG)-treated hyperphagic obese mice had been shown by us earlier to result in anorexia, weight loss, hypoglycemia and subsequent death of all mice. More recent studies suggest that adipose tissue mass may not be the critical determinant of anorexia since a large proportion of GTG-treated non obese (pair-fed to curb obesity) mice when challenged with adrenalectomy also developed anorexia. The aim of the present studies was to determine whether the changes in circulating metabolites, namely, glucose, free fatty acids and hormones, including insulin, glucagon and ACTH, which accompany adrenalectomy, might provide a clue to the causative agent for the onset of anorexia in GTG obese and non obese mice. Accordingly, plasma levels of glucose, free fatty acids, insulin, glucagon and ACTH were measured in GTG-treated obese, non obese and in normal untreated mice following adrenalectomy or a sham operation. Preoperatively, plasma insulin levels were significantly elevated in GTG obese mice whereas plasma glucose, free fatty acids and glucagon levels were not appreciably different than those of untreated controls. Upon adrenalectomy and onset of anorexia, GTG obese mice exhibited a progressive decline in blood glucose and insulin levels; plasma free fatty acids increased precipitously but only after the first day. Plasma glucagon levels declined immediately following adrenalectomy, however, by the 6th day postoperatively they were significantly elevated above the sham operated obese and untreated controls. Prior to adrenalectomy, the pair-fed GTG non obese mice exhibited blood glucose and insulin levels well below the levels of untreated controls and GTG obese mice whereas plasma free fatty acids and glucagon levels were markedly elevated.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

PubMed2004

Obesity-associated hypoventilation in hospitalized patients: prevalence, effects, and outcome.

BACKGROUND: Severe obesity is associated with hypoventilation, a disorder that may adversely affect morbidity and mortality. We sought to determine the prevalence and effects of obesity-associated hypoventilation in hospitalized patients. METHODS: Consecutive admissions to internal medicine services were screened over a 6-month period. In all eligible subjects with severe obesity (body mass index > or =35 kg/m2), we administered a sleep questionnaire, and performed neuropsychological, arterial blood gas, and pulmonary function testing. Hospital course and mortality at 18 months was also determined. RESULTS: Of 4,332 admissions, 6% (n = 277) of patients were severely obese, of whom 150 were enrolled, 75 refused to participate, and 52 met the exclusion criteria. Hypoventilation (mean [+/- SD] arterial partial pressure of carbon dioxide [PaCO2], 52 +/- 7 mm Hg) was present in 31% (n = 47) of subjects who did not have other reasons for hypercapnia. Decreased objective attention/concentration and increased subjective sleepiness were present in patients with obesity-associated hypoventilation compared with in severely obese hospitalized patients without hypoventilation (simple obesity group; mean PaCO2, 37 +/- 6 mm Hg). There were higher rates of intensive care (P = 0.08), long-term care at discharge (P = 0.01), and mechanical ventilation (P = 0.01) among subjects with obesity-associated hypoventilation. Therapy for hypoventilation at discharge was initiated in only 6 (13%) of the patients with obesity-associated hypoventilation. At 18 months following hospital discharge, mortality was 23% in the obesity-associated hypoventilation group as compared with 9% in the simple obesity group (hazard ratio = 4.0; 95% confidence interval: 1.5 to 10.4]. CONCLUSION: Hypoventilation frequently complicates severe obesity among hospitalized adults and is associated with excess morbidity and mortality.

Adult↗

PubMed2005

Obesity and overweight prevalence in Polish 7- to 9-year-old children.

OBJECTIVE: Secular trend in childhood obesity is a well-known phenomenon, and it is important to monitor it in cross-sectional studies. The study aim was to estimate prevalence of obesity and overweight in Polish 7- to 9-year-old children and to compare the results with a French study based on the same protocol. RESEARCH METHODS AND PROCEDURES: The study was conducted in 2001 according to the protocol of the European Childhood Obesity Group. Height and weight were measured, and BMI was calculated to define nutritional status in a randomly selected group of 2916 (1445 girls and 1471 boys) primary school children. Obesity and overweight were estimated according to International Obesity Task Force references with curve for obesity and overweight passing through 30 and 25 kg/m(2) at age 18, respectively. RESULTS: Overweight (including obesity) was found in 15.4% of Polish children (in 15.8% of girls and 15.0% of boys) and obesity in 3.6% (3.7% of girls and 3.6% of boys) compared with 18.1% of overweight and 3.8% of obese children in French study. There was no significant difference in nutrition status between Polish and French children except for higher frequency of overweight in French 9-year-old boys. The same trend of decreasing overweight through age classes was observed in both populations. DISCUSSION: The prevalence of obesity and overweight (including obesity) in prepubertal children estimated in two European countries according to the same protocol and using the same references showed little differences between the two populations despite higher prevalence of obesity in Polish than French adults.

Body Mass Index↗

PubMed1999

The effect of moxonidine on feeding and body fat in obese Zucker rats: role of hypothalamic NPY neurones.

The antihypertensive agent moxonidine, an imidazoline Ii-receptor agonist, also induces hypophagia and lowers body weight in the obese spontaneously hypertensive rat, but the central mediation of this action and the neuronal pathways that moxonidine may interact with are not known. We studied whether moxonidine has anti-obesity effects in the genetically-obese and insulin-resistant fa/fa Zucker rat, and whether these are mediated through inhibition of the hypothalamic neuropeptide Y (NPY) neurones. Lean and obese Zucker rats were given moxonidine (3 mg kg(-1) day(-1)) or saline by gavage for 21 days. Moxonidine decreased food intake throughout by 20% in obese rats (P<0.001) and by 8% in lean rats (P<0.001), and reduced weight gain that final body weight was 15% lower in obese (P<0.001) and 7% lower in lean (P<0.01) rats than their untreated controls. Plasma insulin and leptin levels were decreased in moxonidine-treated obese rats (P<0.01 and P<0.05), but unchanged in treated lean rats. Uncoupling protein-1 gene expression in brown adipose tissue was stimulated by 40-50% (P< or =0.05) in both obese and lean animals given moxonidine. Obese animals given moxonidine showed a 37% reduction in hypothalamic NPY mRNA levels (P = 0.01), together with significantly increased NPY concentrations in the paraventricular nucleus (P<0.05), but no changes in the arcuate nucleus or other nuclei; this is consistent with reduced NPY synthesis in the arcuate nucleus and blocked release of NPY in the paraventricular nucleus. In lean animals, moxonidine did not affect NPY levels or NPY mRNA. The hypophagic, thermogenic and anti-obesity effects of moxonidine in obese Zucker rats may be partly due to inhibition of the NPY neurones, whose inappropriate overactivity may underlie obesity in this model.

Adipose Tissue↗

PubMed1999

Depressed expression of adipocyte beta-adrenergic receptors is a common feature of congenital and diet-induced obesity in rodents.

OBJECTIVE: To determine whether the dramatic reduction in expression and functional activity of the beta3-adrenergic receptor (AR) and beta1AR subtypes originally observed in adipose tissue of the C57BL/6J Lep(ob)/Lep(ob) ('obese') mouse are general features of all models of obesity, and whether obesity-related differences in betaAR subtype expression occur between adipose depots. DESIGN: Survey of adipose tissue betaAR expression from four mouse models of congenital obesity: the 'obese' mouse (C57BL/6J Lep(ob)/Lep(ob)), the 'diabetic' mouse (C57BL/KsJ LepRdb/LepRdb), the 'tubby' mouse (C57BL/6J tub/tub) and the 'fat' mouse (C57BL/KsJ Cpe(fat)/Cpe(fat)), and in a model of high-fat diet-induced obesity in C57BL/6J mice. MEASUREMENTS: Expression of the betaAR subtypes was measured by Northern blot hybridization in white and brown adipose depots. RESULTS: In the severely obese Lep(ob) and LepRdb mice, mRNA concentrations of beta3AR and beta1AR in white adipose tissue (WAT) were decreased by > 99% and by > 70%, respectively. More modest effects on beta3AR expression were observed in brown adipose tissue (BAT, decreased by 20 - 30%). In less severe forms of obesity, as found in the tubby and carboxypeptidase (Cpe)fat mice, and in diet-induced obese B6 mice, beta3AR expression was decreased in WAT by up to 90%, with more modest decreases in interscapular BAT (IBAT). Changes in beta1AR mRNA concentrations were more variable. Beta2AR mRNA levels did not differ in most cases, with the exception that there was a 3-5-fold increase in BAT for both Lep(ob) and LepRdb mice. CONCLUSIONS: Impaired expression of adipocyte betaAR subtypes is a general feature of both genetic and dietary obesity in mice. The degree of obesity is correlated with the extent of loss of beta3AR and beta1AR expression in WAT. The distinct endocrine abnormalities associated with these obesity models may be responsible for the degree of impaired adipocyte betaAR expression.

Adipocytes↗

PubMed2003

Studies of natural allele effects in mice can be used to identify genes causing common human obesity.

Although genes causing rare Mendelian forms of human obesity have provided much useful information about underlying causes of obesity, these genes do not explain significant proportions of common obesity. This review presents evidence that animal models can be used to uncover subtle genetic effects on obesity and can provide a powerful rigorous compliment to human association studies. We discuss the advantages of animal models of obesity, various approaches to discovering obesity genes, and the future of mapping and isolating naturally occurring alleles of obesity genes. We review evidence that it is important to map naturally occurring obesity genes using quantitative trait locus (QTL) mapping, instead of mutagenesis and knockout models because the latter do not allow study of interactions and because naturally occurring obesity alleles can interfere with cloning from mutagenesis projects. Because a substantial percentage of human obesity results from complex interactions, the underlying genes can only be identified by direct studies in humans, which are still very difficult, or by studies in mice that begin with QTL mapping. Finally, we emphasize that animal model studies can be used to prove that a specific gene, only associated with obesity in humans, can indeed be the underlying cause of obesity in mammals.

Animals↗

PubMed1986

Influence of genetic obesity on tissue concentrations of zinc, copper, manganese and iron in mice.

The concentrations (micrograms/gram dry wt) of four essential trace metals in various tissues from C57BL/6J lean (+/?) and obese (ob/ob) mice were determined. Lower concentrations of zinc were found in liver, femur, small intestine and muscle from obese mice than in those from lean mice at 22 wk of age. The concentrations of copper in liver, femur, small intestine, muscle and testes, iron in liver, femur, muscle and plasma, and manganese in liver, femur and small intestine from adult obese mice were also significantly below the concentrations present in tissues from age-matched lean mice. Hepatic concentrations of zinc, copper and manganese in obese mice were also lower than those in lean mice when the different amounts of neutral lipid in obese and lean liver were considered. In contrast with the trend towards lower concentrations of trace metals in tissues from adult obese mice, plasma zinc and copper levels and ceruloplasmin activity were higher in adult obese mice than in lean controls. The effect of genetic obesity on tissue trace metals concentrations was similar in male and female mice. Several tissues from young (5-6 wk of age) obese mice also had lower concentrations of the trace metals than age-matched lean mice, although the differences were not as great as in adults. These data demonstrate that chronic obesity in the genetically obese (ob/ob) mouse is associated with lower concentrations, but not necessarily lower total quantities, of several inorganic micronutrients in tissues. The possibility tht chronic obesity alters the nutritional requirements for these trace metals is discussed.

Animals↗

PubMed2004

Current approaches to obesity management in UK Primary Care: the Counterweight Programme.

BACKGROUND/AIMS: Primary care is expected to develop strategies to manage obese patients as part of coronary heart disease and diabetes national service frameworks. Little is known about current management practices for obesity in this setting. The aim of this study is to examine current approaches to obesity management in UK primary care and to identify potential gaps in care. METHOD: A total of 141 general practitioners (GPs) and 66 practice nurses (PNs) from 40 primary care practices participated in structured interviews to examine clinician self-reported approaches to obesity management. Medical records were also reviewed for 100 randomly selected obese patients from each practice [body mass index (BMI) >/=30 kg m(-2), n = 4000] to review rates of diet counselling, dietetic or obesity centre referrals, and use of anti-obesity medication. Computerized medical records for the total practice population (n = 206 341, 18-75 years) were searched to examine the proportion of patients with a weight/BMI ever recorded. RESULTS: Eighty-three per cent of GPs and 97% of PNs reported that they would raise weight as an issue with obese patients (P < 0.01). Few GPs (15%) reported spending up to 10 min in a consultation discussing weight-related issues, compared with PNs (76%; P < 0.001). Over 18 months, practice-based diet counselling (20%), dietetic (4%) and obesity centre (1%) referrals, and any anti-obesity medication (2%) were recorded. BMI was recorded for 64.2% of patients and apparent prevalence of obesity was less than expected. CONCLUSION: Obesity is under-recognized in primary care even in these 40 practices with an interest in weight management. Weight management appears to be based on brief opportunistic intervention undertaken mainly by PNs. While clinicians report the use of external sources of support, few patients are referred, with practice-based counselling being the most common intervention.

Adolescent↗

PubMed2006

Increased tumor growth in mice with diet-induced obesity: impact of ovarian hormones.

Obesity increases the risk of many cancers in both males and females. This study describes a link between obesity, obesity-associated metabolic alterations, and the risk of developing cancer in male and female mice. The goal of this study was to evaluate the relationship between gender and obesity and to determine the role of estrogen status in obese females and its effect on tumor growth. We examined the susceptibility of C57BL/6 mice to diet-induced obesity, insulin resistance/glucose intolerance, and tumors. Mice were injected sc with one of two tumorigenic cell lines, Lewis lung carcinoma, or mouse colon 38-adenocarcinoma. Results show that tumor growth rate was increased in obese mice vs. control mice irrespective of the tumor cell type. To investigate the effect of estrogen status on tumor development in obese females, we compared metabolic parameters and tumor growth in ovariectomized (ovx) and intact obese female mice. Obese ovx female mice developed insulin resistance and glucose intolerance similar to that observed in obese males. Our results demonstrate that body adiposity increased in ovx females irrespective of the diet administered and that tumor growth correlated positively with body adiposity. Overall, these data point to more rapid tumor growth in obese mice and suggest that endogenous sex steroids, together with diet, affect adiposity, insulin sensitivity, and tumor growth in female mice.

Adenocarcinoma↗

PubMed2005

Impact of obesity and smoking on psoriasis presentation and management.

OBJECTIVE: To study the impact of obesity and smoking on psoriasis. DESIGN: Cross-sectional study. SETTING: University of Utah Department of Dermatology clinics. PATIENTS: A case series of patients with psoriasis enrolled in the prospective Utah Psoriasis Initiative (UPI) (which carefully performs phenotyping of patients with psoriasis) was compared with 3 population databases: the Behavioral Risk Factor Surveillance System of the Utah population, the 1998 patient-member survey from the National Psoriasis Foundation, and 500 adult patients who attend our clinics and do not have psoriasis (non-psoriatic population). RESULTS: The prevalence of obesity in patients within the UPI population was higher than that in the general Utah population (34% vs 18%; P<.001) and higher than that in the non-psoriatic population attending our clinics. Assessment of body image perception with a standardized diagram in the UPI group resulted in the median body image score of normal weight at 18 years of age and the onset of psoriasis, but it changed to overweight at the time of enrollment in the UPI. Thus, obesity appears to be the consequence of psoriasis and not a risk factor for onset of disease. We did not observe an increased risk for psoriatic arthritis in patients with obesity; furthermore, obesity did not positively or negatively affect the response or the adverse effects of topical corticosteroids, light-based treatments, and systemic medications. The prevalence of smoking in the UPI population was higher than in the general Utah population (37% vs 13%; P<.001) and higher than in the non-psoriatic population (37% vs 25%; P<.001). We found a higher prevalence of smokers in the obese population within the UPI than in the obese population within the Utah population (25% vs 9%; P<.001). CONCLUSIONS: Patients with psoriasis attending the University of Utah Dermatology Clinics were more likely to be obese and to smoke compared with non-psoriatic patients and more likely to be obese compared with other large cohorts with psoriasis. Smoking appears to have a role in the onset of psoriasis, but obesity does not. The high prevalence of obesity and smoking in a psoriasis cohort has not been previously noted; if confirmed, it supports the prediction that a significant portion of patients with psoriasis will have the comorbid conditions and public health issues of those with obesity and smoke.

Adrenal Cortex Hormones↗

PubMed1994

Obesity and stature in adolescence and earnings in young adulthood. Analysis of a British birth cohort.

OBJECTIVE: To examine the association between obesity and stature at various ages and earnings in young men and women at age 23 years. DESIGN: We estimated the effect of obesity on earnings by constructing a series of ordinary least-squares regression equations in which the dependent variable was the natural logarithm of hourly earnings at age 23 years. We report the coefficients for obese subjects compared with those for the nonobese subjects and for height while controlling for a number of other factors that are known to affect pay. SETTING: A birth cohort of 12,537 respondents at age 23 years from the National Child Development Study, which consists of all children born in England, Scotland, and Wales between March 3 and 9, 1958. OUTCOME MEASURE: Hourly earnings at age 23 years as it relates to obesity, as determined by the body mass index and stature measured as a continuous variable. RESULTS: Men and women who had been obese at age 16 years had significantly fewer years of schooling than did their nonobese peers. Obese women performed poorly on math and reading tests at ages 7, 11, and 16 years when compared with their nonobese peers. Regression analyses indicated no relationship between obesity at any age and earnings at age 23 years in males. In contrast, there was a statistically significant inverse relation between obesity and earnings in females, independent of parental social class and ability test scores of the child. Female adolescents who were in the top 10% of the body mass index at age 16 years earned 7.4% less (95% confidence interval, -11% to -3.8%) than their nonobese peers; those in the top 1% earned 11.4% less (-21% to -1.5%). The inverse relationship between obesity at 16 years of age and earnings persisted whether the adolescent female remained obese (-6.4% [-12.3% to -4.7%]) or moved into the nonobese category by age 23 years (-7.5% [-12.5% to -2.4%]). A positive relationship was found between height at age 16 years and earnings at age 23 years for men (but not for women) after controlling for social class and IQ. CONCLUSIONS: This study demonstrates an inverse relationship between obesity at 16 years and earnings at age 23 years for British women; the magnitude of the relation is similar to that of other factors that predict earnings, such as gender, job training, and union membership. In the case of men, we found a positive relationship between height and subsequent earnings but no obesity effects.

Adolescent↗

PubMed1997

Cholesterogenesis, lipogenesis, cholesterol degradation to bile acids, and histopathology of the liver in LA/N-cp obese rats.

Various lipid parameters were determined in lean control and LA/NIH-corpulent (LA/N-cp) rats, a normotensive strain showing metabolic characteristics associated with human Type IV hyperlipidemia. Hepatic and plasma total cholesterol, high density lipoproteins (HDL) cholesterol and triglycerides were significantly higher in the obese group than in the control group. Depending upon whether the data were expressed as per gram tissue or per organ, the rates of de novo fatty acid synthesis in the liver and adipose tissue were higher by 61% to 127% (P < .05) and 79% to 355% (P < .05), respectively, in the obese group compared with the lean control group. Similarly, hepatic rate of cholesterol synthesis was higher by 46% to 107% (P < .05) in the obese animals compared with the lean ones. In vivo hepatic rate of HDL2 cholesterol degradation to bile acids was lower in the obese group by 48% to 63% (P < .05). This was confirmed in the perfused liver in spite of the fact that cholesterol uptake from HDL2 was 3- to 4-fold higher in the obese group. These changes in lipid parameters of the obese animals were neither caused by hyperphagia because they were pair-fed with the control group nor caused by increased rate of food consumption because they were meal-fed. At the same time, all these lipid parameters were 17% to 20% higher in ad libitum-fed obese than in pair-fed obese group. Histopathological evaluation of the livers in the obese and control groups also showed prominent lipid droplets in the cytoplasm of the obese liver but not in the lean control liver. Thus, the possible causes of obesity in the LA/N-cp obese rats are higher synthetic rates of lipids coupled with lower rate of degradation of cholesterol to bile acids.

Animals↗

PubMed1994

Hypersensitivity of the corticotropic axis to the serotoninergic agent clomipramine in obese women.

Serotoninergic control of food intake has been shown to be abnormal in obese persons with a decrease in serotoninergic tone. The neuroendocrine effects of intravenous I.V. administration of clomipramine (CMI), a serotonin uptake inhibitor, were studied in normal-weight (n=7) and obese subjects before (n=12) and after (n=6) dietary restriction. Under double-blind, placebo-controlled conditions, a single 12.5 mg dose of CMI was administered. There was no difference in baseline values of prolactin (PRL), corticotropin (ACTH) and cortisol in non-obese controls, obese before and obese after weight loss. CMI led to significant increases of PRL, ACTH, and cortisol concentrations in the controls as well as the obese group. The ACTH and cortisol responses to CMI in obese subjects were somewhat greater than the responses in normal-weight subjects. The area under the curve AUC for ACTH after clomipramine was 6202 +/- 976 pg/ml x 150 minutes for tile obese before weight loss and 3274 +/- 512 pg/ml x 150 minutes for the controls and the difference was significant at the level of p=0.052. The cortisol peak value after clomipramine was 163.71 +/- 14.31 ng/ml in the non-obese and 214.66 +/- 12.59 ng/ml in the obese (p=0.025). However, there was no difference in the obese subjects before and after weight loss. These data support the assumption that obese women have an abnormal sensitivity to the serotoninergic control of the hypothalamic pituitary adrenal axis (HPA), and that a mild weight loss does not significantly modify their serotoninergic tone.

Adolescent↗

PubMed1994

Obesity in minority populations: an epidemiologic assessment.

This article reviews issues relating to the prevalence, health implications, and prevention and treatment perspectives of obesity in U.S racial and ethnic minority groups. The growing interest in obesity in minority populations reflects an awareness of the high prevalence of obesity among black, Hispanic, Asian and Pacific Islander and Native Americans as well as a generally increased interest in minority health. In addition, the fact that some aspects of obesity among minorities differ from those in whites suggests that new insights may be gained from studying obesity in diverse populations. However, there are many methodological problems to be overcome, including some that arise from the way minority groups are defined. Under the assumption that all obesity results from a period of sustained positive energy balance at the individual level, an epidemiologic explanation for the excess of obesity in minorities at the population level seems readily apparent. A surplus of obesity-promoting forces and a deficit of obesity-inhibiting forces, caused by secular changes in food availability and physical activity, accompany the early phases of modernization and economic advancement. The high prevalence of obesity in minority populations can be viewed as a function of the slope and timing of these secular changes. Genetic predisposition, cultural attitudes, and exposure to maternal obesity and diabetes in utero may be potentiating factors. In this context, interventions targeting individuals would seem inevitably to put racial and ethnic minority groups on the path toward the same weight control crisis now observed in the majority white population. This suggests that the underlying causes of the societal energy balance problem must be addressed at the population level in order for effective clinical approaches to be developed for minority populations with a high obesity prevalence.

Adult↗

PubMed1997

Dietary intake in relation to restrained eating, disinhibition, and hunger in obese and nonobese Swedish women.

The aims of this study were to: describe dietary intakes of obese and nonobese middle-aged women using a validated food frequency questionnaire; to assess dietary restraint, disinhibition, and hunger by the three factor eating questionnaire (TFEQ) in obese and nonobese samples and determine which of the factors are independently associated with obesity; and to examine correlations between selected nutritional variables and the TFEQ factors. Subjects studied included 179 obese Swedish women (BMI > 32) and 147 nonobese population-based controls (BMI < 28). Age-adjusted mean energy intake was significantly higher in obese women (2730 +/- 78 vs. 2025 +/- 85 kcal, p < 0.0001). In absolute and relative terms, fat intake was higher and alcohol intake was lower in the obese subjects. Disinhibition was the strongest TFEQ factor independently differentiating the obese and nonobese states, i.e., after adjustment for restraint and hunger. Within the obese sample, strong associations were seen between energy intake and disinhibition (p = 0.0005) and hunger (p = 0.0004). The association between energy intake and restrained eating was negative and weaker (p = 0.04). No such associations were seen in nonobese women. Thus, using a dietary instrument that is valid and unbiased with respect to obesity, strong psychological correlates, possibly causal, of variability in energy intake were detected in middle-aged women with obesity. Disinhibition is associated with both obesity and high-energy intakes and is therefore an important factor to consider in the treatment of women with obesity.

Adult↗

PubMed1998

The case for medical management of obesity: a call for increased physician involvement.

The United States is in the midst of an escalating epidemic of obesity. Over one-third of the adult population in the United States is currently obese and the prevalence of obesity is growing rapidly. By any criteria, obesity represents a chronic disease which is associated with a wide range of comorbidities, including coronary heart disease (CHD), Type 2 diabetes, hypertension and dyslipidemias. The comorbidities of obesity are common, occurring in over 70% of individuals with a BMI of > or = 27. In addition to obesity itself, excessive accumulation of visceral abdominal fat and significant adult weight gain also represent health risks. Physicians have an important role to play in the treatment of obesity. Unfortunately, the medical community has not been involved actively enough to help stem the major epidemic of obesity occurring in the United States. This article puts forth a proposed model for the treatment of obesity in clinical practice, including obtaining the "vital signs" of obesity, recommending lifestyle measures, and instituting pharmacologic therapy when appropriate. By utilizing a chronic disease treatment model, physicians can join other health care professionals to effectively treat the chronic disease of obesity. Relatively modest weight loss, on the order of 5-10% of initial body weight can result in significant health improvements for many patients and represent an achievable goal for most obese patients.

Adult↗

PubMed1983

Energy fuel and hormonal profile in experimental obesities.

Several types of experimental obesities are characterized by the occurrence of an early hypersecretion of insulin that produces an increase in both triglyceride secretion by the liver and fat deposition in adipose tissue. This hypersecretion of insulin, together with other ill-defined factors, is subsequently responsible for a state of insulin resistance. The early oversecretion of insulin in hypothalamic and genetic (e.g. fa/fa rats) obesities can be experimentally demonstrated. Thus, within 20 min of acute lesion of the ventromedial hypothalamus (VMH), glucose-induced insulin secretion is greater in lesioned than in non-lesioned control rats; this increase can be blocked by superimposed, acute vagotomy. Moreover, an infusion of glucose to 17-day-old, pre-weaned control and genetically pre-obese rats (i.e. animals genetically-determined to become obese but with a normal body weight at this age) elicits much greater insulinaemia in the pre-obese than in the controls, despite similar basal, pre-infusion values in both. This increased insulin secretion in the pre-obese rats can be restored to normal by pre-treating them acutely with the cholinergic inhibitor, atropine. Thus, in these two types of obesity, an increased vagal tone appears to be of importance for the early occurrence of insulin over-secretion. Hyperinsulinaemia produced by increased tone of the vagus nerve appears to be reinforced by the decreased activity of the sympathetic system observed in obese rodents. In many obese rodents, plasma growth hormone levels are abnormally low. The inadequate secretion of this hyperglycaemic hormone may explain why, in some types of obesity syndrome, hyperglycaemia is not necessarily present, despite insulin resistance. Insulin resistance in experimental obesities has been shown to occur at the level of the adipose tissue, the muscles and more recently, the liver. The latter has been demonstrated using the in vivo euglycaemic clamp technique; thus, glycogenolysis of genetically obese (fa/fa) rats could not be shut off, as in controls, by either basal or increased plasma insulin levels. This particular pathway is therefore insulin resistant. The precise etiology of the early over-secretion of insulin in VMH-lesioned rats is, however, unknown: with VMH lesions, the origin is clearly the central nervous system (CNS), but the pathways actually interrupted by the lesions and those responsible for the hyperactivity of the vagus, remain to be determined.(ABSTRACT TRUNCATED AT 400 WORDS)

Adipose Tissue↗

PubMed1983

Does obesity explain excess prevalence of diabetes among Mexican Americans? Results of the San Antonio Heart Study.

Obesity and Type 2 (non-insulin-dependent) diabetes mellitus are common in the Mexican American population. It is not clear whether this is merely a specific instance of the more general phenomenon of excess Type 2 diabetes and obesity among poor people, or whether Mexican Americans have a discrete genetic susceptibility to Type 2 diabetes. The latter consideration arises because Mexican Americans are of mixed native American and European ancestry and native Americans may have a genetic predisposition to Type 2 diabetes which Mexican Americans could share. We studied 936 Mexican Americans and 398 Anglo-Americans randomly selected from three socially and culturally distinct neighborhoods in San Antonio, Texas. Three categories of obesity--lean, average, and obese--were defined using the Anglo-American distribution of the sum of the triceps and subscapular skinfold. Mexican Americans were two to four times as likely to fall into the obese category as Anglo-Americans, but within categories, the two ethnic groups were closely matched in terms of sum of skinfolds. The prevalence of Type 2 diabetes, however, was significantly greater in Mexican Americans than in Anglo-Americans even when the comparisons were made within the three obesity categories. The summary prevalence ratio, controlling for obesity, was 2.54 for men (p = 0.004) and 1.70 for women (p = 0.036). Thus, lean Mexican Americans are still at greater risk of Type 2 diabetes than equally lean Anglo-Americans. Conversely, although Type 2 diabetes prevalence increases as expected with increasing obesity in both ethnic groups, obese Anglo-Americans are still relatively protected compared with equally obese Mexican Americans. Plasma glucose was significantly higher in Mexican Americans than in Anglo-Americans even after controlling for obesity. These results indicate that, although obesity contributes to Type 2 diabetes in Mexican Americans, it does not by itself explain the entire excess prevalence rate.

Adult↗