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PubMed1984

The relationship between energy expenditure and environmental temperature in congenitally obese and non-obese Zucker rats.

The energy expenditure of normal and congenitally obese adult female Zucker rats has been measured by continuous indirect calorimetry for periods of 3-10 days at ambient temperatures varied from 30 to 5 degrees C. Rectal temperatures were also recorded. Exposure to cold caused no ill-effects in normal or obese rats. The rectal temperatures of obese rats were about 1 degree C lower than those of normal rats. The rectal temperatures of normal rats did not change measurably with ambient temperature; in obese rats rectal temperature rose slightly as ambient temperature fell. In normal and obese rats, energy expenditure showed a smooth, steeply sloping, negative relationship to ambient temperature. Energy expenditure per rat was higher in obese than in normal rats at all temperatures. The two slightly curvilinear regressions were nearly 'parallel', with a separation of about 40 kJ/day per rat at the mid-point. This study therefore does not confirm suggestions that obese Zucker rats suffer from a defect in the level of energy expenditure, or in their capacity to increase it when exposed to cold. It is suggested that in both normal and obese rats the level of energy expenditure was determined by thermoregulatory control. The greater heat production of obese rats may have been a response to their lower core temperature. A steady state in which greater heat production is associated with lower core temperature implies lower insulation between body core and surface. This could be due to greater blood flow.

Animals↗
PubMed2007

Maternal obesity increases hypothalamic leptin receptor expression and sensitivity in juvenile obesity-prone rats.

In rats selectively bred to develop diet-induced obesity (DIO) or to be diet-resistant (DR), DIO maternal obesity selectively enhances the development of obesity and insulin resistance in their adult offspring. We postulated that the interaction between genetic predisposition and factors in the maternal environment alter the development of hypothalamic peptide systems involved in energy homeostasis regulation. Maternal obesity in the current studies led to increased body and fat pad weights and higher leptin and insulin levels in postnatal day 16 offspring of both DIO and DR dams. However, by 6 wk of age, most of these intergroup differences disappeared and offspring of obese DIO dams had unexpected increases in arcuate nucleus leptin receptor mRNA, peripheral insulin sensitivity, diet- and leptin-induced brown adipose temperature increase and 24-h anorectic response compared with offspring of lean DIO, but not lean DR dams. On the other hand, while offspring of obese DIO dams did have the highest ventromedial nucleus melanocortin-4 receptor expression, their anorectic and brown adipose thermogenic responses to the melanocortin agonist, Melanotan II (MTII), did not differ from those of offspring of lean DR or DIO dams. Thus, during their rapid growth phase, juvenile offspring of obese DIO dams have alterations in their hypothalamic systems regulating energy homeostasis, which ameliorates their genetic and perinatally determined predisposition toward leptin resistance. Because they later go onto become more obese, it is possible that interventions during this time period might prevent the subsequent development of obesity.

Adipose Tissue↗
PubMed1990

Effects of antiglucocorticoid RU 486 on development of obesity in obese fa/fa Zucker rats.

The effects of RU 486 (mitepristone), an antagonist of type II glucocorticoid receptors (GR), on the development of obesity in young 5-wk-old obese fa/fa rats has been investigated. After 15 days of treatment, body composition of obese RU 486-treated rats was similar to that of lean-vehicle rats. Analysis of body composition changes showed that RU 486 effectively reversed the obesity. It stopped fat deposition in obese rats but increased protein deposition to the level of lean-vehicle rats. RU 486 prevented the development of hyperphagia and reduced gross energetic efficiency in the obese rats but had little effect on lean rats. Brown adipose tissue mitochondrial GDP binding was increased in obese rats but was reduced in lean rats by RU 486 treatment. RU 486 also reduced the elevated activity of hippocampal glycerophosphate dehydrogenase, a glucocorticoid-responsive enzyme, of obese rats to the level of lean rats. The evidence suggests that abnormal activity of glucocorticoid GR receptors or abnormal cellular responsiveness to corticosterone receptor complexes may be important in the development of obesity in the fa/fa rat.

Animals↗
PubMed1988

Role of obesity and hyperinsulinemia in the insulin resistance of obese subjects with the clinical triad of polycystic ovaries, hirsutism and acanthosis nigricans.

The insulin resistance of 4 nonobese and 8 obese patients with polycystic ovaries, hirsutism and benign acanthosis nigricans, and of 6 'obese normal' apart from obesity and 10 normal female subjects was evaluated by means of an intravenous insulin tolerance test and by measuring basal and insulin responses to an oral glucose load. The patients with polycystic ovaries, hirsutism and acanthosis had a decreased hypoglycemic response to exogenous insulin. The subjects with polycystic ovaries presented a significantly greater mean glucose response area for the same or greater mean insulin response area than the obese or nonobese normal subjects. The insulin resistance in the patient with polycystic ovaries, hirsutism and acanthosis nigricans could not be exclusively ascribed to a reduced receptor number, but also appeared to be due to a simultaneous postbinding defect probably related to the high insulin levels in patients with polycystic ovaries be they obese or not. The elevated plasma androgens and the presence of acanthosis found in these patients are likely also related to the hyperinsulinemia. To evaluate the influence of obesity, obese and nonobese patients with acanthosis nigricans and polycystic ovaries were compared. Higher insulin levels were found in the thin subjects, which could explain their greater insulin resistance and more severe hyperandrogenism. The comparison between obese patients with and those without acanthosis nigricans and polycystic ovaries suggested that, despite similar insulin levels, the greater known duration of obesity (probably also of the hyperinsulinemia) of the former was a possible explanation for their more intense insulin resistance and higher testosterone levels.

Acanthosis Nigricans↗
PubMed1985

Noninvasive study of left ventricular performance in obese patients: influence of duration of obesity.

We studied the performance of the left ventricle in 35 obese patients by means of noninvasive methods, including echocardiography, carotid arterial pulse tracing, and phonocardiography. Patients were divided into two groups according to the duration of obesity: group 1 included patients who had been obese for less than 15 years, and group 2 comprised patients who had been obese for more than 15 years. There were no differences in the degree of obesity and cellularity of adipose tissue between two groups. Left ventricular dimension and wall thickness, stroke volume, and cardiac output were significantly greater in both groups of obese patients than in nonobese control subjects. Group 2 had a significantly increased end-diastolic dimension index (DdI, calculated as end-diastolic dimension/cube root of body surface area), stroke index (SI), and radius/wall thickness ratio (R/Th) of the left ventricle compared with group 1. Multiple regression analysis showed that DdI, SI, and R/Th correlated significantly with the duration of obesity. We conclude that alterations of cardiac performance in obese patients with left ventricular enlargement and wall thickening is attributed not only to the excess of body weight but also to the duration of obesity.

Adolescent↗
PubMed2003

Obese Zucker rats have reduced mineralocorticoid receptor and 11beta-hydroxysteroid dehydrogenase type 1 expression in hippocampus-implications for dysregulation of the hypothalamic-pituitary-adrenal axis in obesity.

Obese Zucker rats have elevated basal corticosterone levels and an increased stress response suggestive of an increased activity of the hypothalamic-pituitary-adrenal (HPA) axis. We hypothesized that altered central expression of glucocorticoid receptors (GR), mineralocorticoid receptors (MR), and/or 11beta-hydroxysteroid dehydrogenase type 1 (11betaHSD1) contribute to these changes. In brains from young adult male rats, in situ hybridization and Western blotting showed that obese rats had normal hippocampal GR mRNA and protein levels. In contrast, in obese rats, 11betaHSD1 mRNA levels were reduced in a subpopulation of hippocampal cells in the main neuronal layers (by 37-47%, P < 0.05), whereas 11betaHSD1 levels in sparse high-expressing cells did not differ. MR mRNA was decreased in all regions of the hippocampus (by 37-49%, P < 0.05 for CA1-2 and P < 0.01 for dentate gyrus) and in frontal cortex (by 16%, P < 0.05) in obese rats. In whole hippocampal homogenates, however, neither the protein concentration of MR by Western blot nor activity of 11betaHSD1 was measurably different between the phenotypes. To test the functional importance of lower central MR expression, groups of lean and obese rats were given spironolactone before restraint stress. In vehicle-treated animals, obese rats had higher plasma corticosterone levels than lean rats after stress (by ANOVA, P < 0.05). Spironolactone markedly increased the corticosterone response in both groups, but the incremental rise was smaller in the obese rats, so that spironolactone abolished the differences between groups. We conclude that lower levels of MR, but not GR, contribute to the increased HPA activity in the obese Zucker rats and that this seems more influential during stress than in the basal state. This may be exacerbated by impaired local regeneration of corticosterone by 11betaHSD1. These abnormalities could contribute to the subtle changes in the HPA axis in rodent and human obesity.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1993

Suppression of GLUT4 expression in skeletal muscle of rats that are obese from high fat feeding but not from high carbohydrate feeding or genetic obesity.

In this study we determined whether alterations in the expression of GLUT4, the major insulin-regulatable glucose transporter, in skeletal muscle could explain the insulin-resistant glucose uptake characteristic of both dietary-induced and genetic obesity. GLUT1 expression was measured for comparison. To assess glucose transporter protein levels in dietary-induced obesity, postnuclear membranes were prepared from hindlimb muscle of Sprague-Dawley rats fed chow ad libitum (control), a high calorie/carbohydrate diet, or a high fat (80%) diet for 7 weeks. Immunoblotting revealed that GLUT4 protein levels decreased 34% in high fat-fed rats, but were unaltered in high calorie/carbohydrate-fed obese rats compared to control values. GLUT4 mRNA per DNA decreased 47% in muscle of high fat-fed rats compared to that in control or high calorie-fed rats; GLUT1 mRNA was reduced 31%, and actin mRNA tended to decrease (29%). To assess GLUT4 and GLUT1 expression in genetic obesity, similar studies were carried out in 5- and 20-week-old lean and obese Zucker rats as well as in 20-week-old obese Zucker rats 36 h after streptozotocin injection to lower insulin levels. GLUT4 protein and mRNA levels were unaltered in hindlimb muscle of obese Zucker rats at either age or in the acutely diabetic state, whereas GLUT1 protein and mRNA levels decreased 40-45%. Comparison of these results with recent data in adipocytes demonstrates tissue-specific regulation of expression of GLUT4 and GLUT1. Thus, obesity due to high fat feeding, but not that due to high calorie/carbohydrate feeding or genetics, is associated with pretranslational suppression of GLUT4 expression in skeletal muscle. In at least some forms of obesity, the level of GLUT4 expression in muscle appears to be only one factor in, or may even be unrelated to, the degree of insulin-responsive glucose transport in vivo.

Actins↗
PubMed2006

ENPP1 variants and haplotypes predispose to early onset obesity and impaired glucose and insulin metabolism in German obese children.

CONTEXT: ENPP1 (nucleotide pyrophosphatase/phosphodiesterase-1) encodes a membrane-bound glycoprotein that inhibits the insulin-receptor tyrosine kinase activity, resulting in reduced insulin sensitivity. Hence, variants in this gene may be related to obesity and insulin resistance. OBJECTIVE: Therefore, in this study, we aimed to explore the role of ENPP1 genetic variants in obesity and related traits in a representative population of Caucasian children and in cohorts of obese children with detailed metabolic characteristics including oral glucose tolerance test. DESIGN: We genotyped the K121Q, IVS20delT-11, and A/G+1044TGA ENPP1 genetic variants for association analyses in 712 schoolchildren (346 boys and 366 girls; mean age 12 +/- 3 yr; mean body mass index-sd score 0.09 +/- 0.04) and in independent cohorts of 205 obese children from Leipzig and 195 obese children from Datteln, Germany. RESULTS: We identified a significantly increased risk of obesity in Leipzig children carrying the 121Q variant (adjusted odds ratio, 1.82; 95% confidence interval, 1.30-2.56; P = 0.0005) or the [Q-delT-G] haplotype [1.75 (1.17-2.62), P = 0.006] as compared with a lean control group. This was replicated in another independent obesity/overweight cohort from Leipzig as well as obese children from Datteln. In addition, obese children from Leipzig with the [Q-delT-G] haplotype were characterized by impaired glucose metabolism, whereas the [K-delT-G] and [K-insT-A] haplotypes were significantly associated with improved insulin sensitivity and glucose metabolism (all P < 0.05 after adjusting for age, gender, and body mass index). CONCLUSIONS: In conclusion, our study suggests a potential role of the K121Q polymorphism or derived ENPP1 haplotypes in increased susceptibility to obesity and early impairment of glucose and insulin metabolism in children.

Adolescent↗
PubMed2006

Obesity and sex steroid changes across puberty: evidence for marked hyperandrogenemia in pre- and early pubertal obese girls.

CONTEXT: Peripubertal obesity is associated with abnormal sex steroid concentrations, but the timing of onset and degree of these abnormalities remain unclear. OBJECTIVE: The objective of the study was to assess the degree of hyperandrogenemia across puberty in obese girls and assess overnight sex steroid changes in Tanner stage 1-3 girls. DESIGN: This was a cross-sectional analysis. SETTING: The study was conducted at general clinical research centers. SUBJECTS: Thirty normal-weight (body mass index for age < 85%) and 74 obese (body mass index for age >or= 95%) peripubertal girls. INTERVENTION: Blood samples (circa 0500-0700 h) were taken while fasting. Samples from the preceding evening (circa 2300 h) were obtained in 23 Tanner 1-3 girls. MAIN OUTCOME MEASURES: Hormone concentrations stratified by Tanner stage were measured. RESULTS: Compared with normal-weight girls, mean free testosterone (T) was elevated 2- to 9-fold across puberty in obese girls, whereas fasting insulin was 3-fold elevated in obese Tanner 1-3 girls (P < 0.05). Mean LH was lower in obese Tanner 1 and 2 girls (P < 0.05) but not in more mature girls. In a subgroup of normal-weight Tanner 1-3 girls (n = 17), mean progesterone (P) and T increased overnight 2.3- and 2.4-fold, respectively (P <or= 0.001). In obese Tanner 1-3 girls (n = 6), evening P and T were elevated, and both tended to increase overnight [mean 1.4- and 1.6-fold, respectively (P = 0.06)]. CONCLUSIONS: Peripubertal obesity is associated with hyperandrogenemia and hyperinsulinemia throughout puberty, being especially marked shortly before and during early puberty. P and T concentrations in normal-weight Tanner 1-3 girls increase overnight, with similar but less evident changes in obese girls.

Adolescent↗
PubMed1989

Cholinergic receptor activation by pyridostigmine restores growth hormone (GH) responsiveness to GH-releasing hormone administration in obese subjects: evidence for hypothalamic somatostatinergic participation in the blunted GH release of obesity.

GH secretion in response to provocative stimuli is decreased in obese individuals. However, the precise mechanism causing this decrease is unknown. In an attempt to determine if reduced cholinergic stimulation accounts for the decreased GH secretion, we studied the effect of enhanced cholinergic tone induced by pyridostigmine on GHRH-stimulated GH secretion in a group of seven obese and seven normal subjects. When GHRH (100 micrograms, iv) was administered after placebo in the obese group, mean plasma GH rose from 0.5 +/- (0.1 (+/- SE) to 3.6 +/- 1.5 micrograms/L at 30 min. When the same obese subjects were given GHRH 60 min after pyridostigmine administration (120 mg, orally), the mean plasma GH level rose from 1.8 +/- 0.6 to 21.0 +/- 7.5 micrograms/L at 30 min. The responses to placebo and pyridostigmine were significantly different at 15, 30, 45, 60, and 90 min. In the normal subjects, a similar dose of GHRH induced a GH peak of 24.3 +/- 7.1 micrograms/L, and the GHRH-stimulated peak was significantly higher (56.2 +/- 16.8 micrograms/L) after pyridostigmine administration. To study the effect of pyridostigmine alone six other obese and six other normal subjects were tested with pyridostigmine or placebo on different days. In the normal subjects the mean peak plasma GH level after pyridostigmine was 12.5 +/- 3.1 micrograms/L, and in the obese subjects it was 4.6 +/- 1.3 micrograms/L. Thus, pyridostigmine potentiated the action of GHRH, rather than merely being additive. We conclude that pyridostigmine stimulates GH secretion in obese as well as normal subjects, although the response was less in the former group. Pyridostigmine potentiates the response to GHRH in both groups, but again, the response was less in the obese subjects. These results suggest that the impaired somatotroph responsiveness in obese subjects may be due to chronically decreased hypothalamic cholinergic tone, resulting in enhanced somatostatinergic tone.

Adolescent↗
PubMed1996

The involvement of the opioid system in human obesity: a study in normal weight relatives of obese people.

The involvement of the opioid system in human obesity has been demonstrated, but whether the abnormalities in the endorphinergic system play a primary role in overfeeding and weight gain or represent a simple biochemical feature is still unclear. The objectives of this study were to investigate the effects of both physiological and pharmacological plasma beta-endorphin levels on some metabolic and hormonal parameters in a normal weight, but prone to obesity, young population consisting of first degree relatives of obese subjects and in body mass index-, sex, and age- matched control subjects without a family history of obesity. Each subject underwent a 1-h infusion of synthetic human beta-endorphin at a constant rate of 4.5 ng/kg.min (low rate), then after a 1-week interval, at a rate of 500 micrograms/h (high rate). Under basal conditions, there was no significant difference in plasma glucose and pancreatic hormones (insulin, C peptide, and glucagon) between the two groups, except for plasma beta-endorphin levels, which were significantly (P < 0.01) higher in relatives of obese individuals. The low rate of beta-endorphin infusion induced physiological elevations of plasma opioid levels in both groups; no significant change in plasma glucose and pancreatic products in control subjects; and a significant (at least P < 0.05) rise in plasma insulin, C peptide, and glucagon concentrations in relatives of the obese. The high rate of beta-endorphin infusion produced pharmacological elevations of opioid plasma levels in both groups; significant (at least P < 0.05) increments in plasma glucose and glucagon levels and no appreciable modification of plasma insulin and C peptide levels in the control group; and a significant (at least P < 0.05) positive response of plasma glucose, insulin, C peptide, and glucagon levels in relatives of obese subjects. These findings suggest that 1) opioid peptides at least in part play a primary, rather than secondary, role in some metabolic events of obesity; and 2) both physiological and pharmacological plasma levels of beta-endorphin are able to provoke marked islet hormone release in the early phase of human obesity.

Adult↗
PubMedDate not supplied

Tissue oxygenation in obese and non-obese patients during laparoscopy.

BACKGROUND: Wound infection risk is inversely related to subcutaneous tissue oxygenation, which is reduced in obese patients and may be reduced even more during laparoscopic procedures. METHODS: We evaluated subcutaneous tissue oxygenation (PsqO(2)) in 20 patients with a body mass index (BMI) > or=40 kg/m(2) (obese group) and 15 patients with BMI <30 kg/m(2) (non-obese group) undergoing laparoscopic surgery with standardized anaesthesia technique and fluid administration. Arterial oxygen tension was maintained near 150 mmHg. PsqO(2) was measured from a surrogate wound on the upper arm. RESULTS: A mean FIO(2) of 51% (13%) was required in obese patients to reach an arterial oxygen tension of 150 mmHg; however, a mean FIO(2) of only 40% (7%) was required to reach the same oxygen tension in non-obese patients (P=0.007). PsqO(2) was significantly less in obese patients: 41 (10) vs 57 (15) mmHg (P<0.001). CONCLUSION: Obese patients having laparoscopic surgery require a significantly greater FIO(2) to reach an arterial oxygen tension of about 150 mmHg than non-obese patients; they also have significantly lower subcutaneous oxygen tensions. Both factors probably contribute to an increased infection risk in obese patients.

Adult↗
PubMed2001

Postprandial triglyceridemia in obese and non-obese adolescents. Importance of body composition and fat distribution.

BACKGROUND: It has recently been shown that obese adults have a disturbed metabolism of postprandial lipoproteins, resulting in postprandial hypertriglyceridemia. To the best of our knowledge, there are no data about postprandial triglyceridemia in obese and non-obese children and adolescents. SUBJECTS: 12 obese and 12 non-obese adolescents, aged 11.0 to 13.8 years. METHODS: Body composition and fat distribution (waist-to-hip circumference ratio and triceps/ subscapular skinfold thickness ratio) were assessed by anthropometry. An oral fat tolerance test was carried out, and fasting and postprandial lipid-lipoprotein serum concentrations were measured. RESULTS: We observed a significant increase in triglyceride serum concentrations 2 and 4 hours after the oral fat load, in both obese and non-obese adolescents. In obese and non-obese adolescents there were significant correlations between some variables of postprandial lipemia and the studied indices of body fat distribution. When we compare postprandial lipemia in adolescents having a central pattern of fat distribution with those having a peripheral pattern of fat distribution, we observed higher variables related to postprandial lipemia in those having a central pattern of fat distribution compared with those with a peripheral pattern (sum of serum triglyceride concentrations: 6.06 vs 4.41, p = 0.0243). CONCLUSIONS: We present a protocol to study postprandial lipemia in children and adolescents that allowed us to observe significant changes after an oral fat load. Results obtained indicate that the pattern of distribution of adipose tissue may be more important for lipid metabolism disturbances than total adipose tissue per se.

Adipose Tissue↗
PubMed2005

Plasma calcitonin gene-related peptide is increased prior to obesity, and sensory nerve desensitization by capsaicin improves oral glucose tolerance in obese Zucker rats.

OBJECTIVE: It has earlier been demonstrated that capsaicin-induced desensitization improves insulin sensitivity in normal rats. However, whether increased capsaicin-sensitive nerve activity precedes the onset of insulin resistance in diet-induced obesity--and therefore might be involved in the pathophysiology--is not known. Further, it is of relevance to investigate whether capsaicin desensitization improves glycaemic control even in obese individuals and we therefore chose the obese Zucker rats to test this. DESIGN AND METHODS: Plasma levels of calcitonin gene-related peptide (CGRP; a marker of sensory nerve activity) was assessed in 8-week-old Zucker rats. To investigate whether capsaicin desensitization (100 mg/kg at 9 weeks of age) would also ameliorate glycaemia in this non-diabetic model, we assessed oral glucose tolerance at 7 weeks after capsaicin. RESULTS: It was found that plasma CGRP levels were elevated in obese Zucker rats prior to the onset of obesity (16.1+/-3.4 pmol/l in pre-obese Zucker rats vs 6.9+/-1.1 pmol/l in lean littermates; P = 0.015) despite similar body weights. Furthermore, capsaicin desensitization reduced both fasting blood glucose (4.3+/-0.2 mmol/l vs 5.1+/-0.2 mmol/l in controls; P = 0.050) as well as the mean blood glucose level during an oral glucose tolerance test (OGTT) (6.8+/-0.3 mmol/l vs 8.6+/-0.5 mmol/l in control obese rats; P = 0.024) whereas the plasma insulin levels during the OGTT were unchanged. However this did not lead to an improvement in insulin resistance or to a reduction of tissue triglyceride accumulation in muscle or liver. CONCLUSION: We concluded that capsaicin-induced sensory nerve desensitization improves glucose tolerance in Zucker rats. Since, in this study, plasma CGRP levels, a marker of sensory nerve activity, were increased in the pre-obese rats, our data support the hypothesis that increased activity of sensory nerves precedes the development of obesity and insulin resistance in Zucker rats.

Animals↗
PubMed2002

Assessing risk factors for obesity between childhood and adolescence: I. Birth weight, childhood adiposity, parental obesity, insulin, and leptin.

OBJECTIVE: To assess the effects of body weight, body composition, parental obesity, and metabolic variables on the development of obesity in a large cohort of 5-year-old Native American children with a high propensity for obesity. METHODS: During the summer months of 1992 to 1995 and again 5 years later, 138 (65 boys and 73 girls) 5-year-old Pima Indian children were studied. Height; weight; body composition; parental obesity; and fasting plasma insulin, glucose, and leptin concentrations were determined at baseline and follow-up. Linear regression models were used to assess the effect of the baseline variables on the development of obesity. RESULTS: At both 5 and 10 years of age, Pima Indian children were heavier and fatter than an age- and gender-matched reference population. All anthropometric and metabolic variables tracked strongly from 5 to 10 years of age (r > or = 0.70). The most significant determinant of percentage of body fat at 10 years of age was percentage of body fat at 5 years of age (R(2) = 0.53). The combined effect of high maternal body mass index, elevated fasting plasma leptin concentrations, and low fasting plasma insulin concentrations at baseline explained an additional 4% of the total variance in adiposity at follow-up. CONCLUSIONS: Although parental obesity and metabolic variables such as insulinemia and leptinemia at baseline account for a small percentage of the variance in adiposity at follow-up, early childhood obesity is the dominant predictor of obesity 5 years later. These results suggest that strategies to prevent childhood obesity must be initiated at a very early age.

Adipose Tissue↗
PubMed2005

Determination of risk factors in obese and non-obese patients with coronary artery disease.

OBJECTIVE: Obesity is a complex multifactorial chronic disorder recently classified by the American Heart Association (AHA) as a modifiable risk factor for coronary artery disease (CAD). This study was designed to assess conventional and novel risk factors in obese and non-obese patients with CAD. METHODS AND RESULTS: This study evaluates the association between conventional and novel coronary risk factors and CAD in obese and non-obese patients by using multivariate stepwise logistic regression analysis. The obese CAD group was identified by the following predictors of CAD: age, sex, hypertension, diabetes mellitus, smoking, family history of CAD, low level of HDL cholesterol, high LDL cholesterol, high C-reactive protein, high homocysteine. In a non-obese CAD group, the identified predictors of CAD were age, sex, hypertension, smoking, family history of CAD, levels of high C-reactive protein, and high homocysteine. Hypertension was found to be the strongest predictor for both obese (OR: 39.91, 95% confidence intervals (CI): 5.5 1-280.3, p < 0.001) and non-obese (OR: 14.39, 95% CI: 4.4-25.8, p < 0.001) patients with CAD. CONCLUSIONS: From our data, we conclude that hypertension appears to be the strongest independent predictor of CAD regardless of body mass index (BMI).

Age Distribution↗
PubMed1989

Increased basal glucose production and utilization in children with recent obesity versus adults with long-term obesity.

To characterize the abnormalities of glucose homeostasis and insulin action early in the course of human obesity, we studied in vivo glucose kinetics in seven children who were recently massively overweight. At time of study they were gaining weight at a rate of 13.5 +/- 1.4 kg/yr. They were compared with six age-matched control subjects. Six adults with long-term obesity and five normal adults were studied in parallel. The obese children and adults were normoglycemic and hyperinsulinemic. We found that glucose production and utilization were remarkably higher in obese children (295 +/- 18 mg/min; 7.6 mg.kg-1 lean body mass.min-1) than in control children (129 +/- 13 mg/min; 4.4 mg.kg-1 lean body mass.min-1, P less than .01) and obese adults (151 +/- 8 mg/min; 3.1 +/- 0.3 mg.kg-1 lean body mass.min-1, P less than .01). Obese adults had normal rates of glucose production and utilization. Insulin- and non-insulin-mediated glucose uptake, estimated with somatostatin-induced suppression of endogenous insulin secretion, contributed almost equally to the excess glucose utilization observed in the obese children. When studied with the euglycemic-hyperinsulinemic clamp, obese children could not increase glucose disposal to the same extent as normal children and were not able to adequately suppress their endogenous glucose production. Recently obese children are therefore characterized by an increased basal glucose turnover rate and an already established insulin resistance of the liver and probably the skeletal muscles.

Adipose Tissue↗
PubMed2001

Identification of novel genes differentially expressed in omental fat of obese subjects and obese type 2 diabetic patients.

Obesity is associated with an increased risk for developing type 2 diabetes, insulin resistance, hypertension, dyslipidemia, cardiovascular disease, respiratory dysfunction, and certain forms of cancer. Insulin resistance in many type 2 diabetic patients is the result of increased visceral adiposity. To identify novel genes implicated in type 2 diabetes and/or obesity and to elucidate the molecular mechanisms underlying both diseases, we analyzed gene expression in omental fat from lean and obese nondiabetic subjects and obese type 2 diabetic patients using mRNA differential display and subtracted library techniques. After screening over 13,800 subtracted cDNA clones and 6,912 cDNA amplification products, we identified 2,078 cDNAs that showed potential differential expression in the omental fat of lean versus obese nondiabetic subjects versus obese type 2 diabetic patients. Data analysis showed that 70.7% of these clones corresponded to unknown genes (26.7% matched express sequence tags [ESTs]) and 29.3% corresponded to known genes. Reverse Northern and classic Northern analyses further confirmed that the expression of five of these cDNA clones was elevated in obese nondiabetic subjects and obese type 2 diabetic patients. Four candidate genes were further evaluated for tissue distribution, which showed expression primarily in adipose and skeletal muscle tissue, and chromosomal localization. We concluded that both mRNA differential display and subtracted cDNA libraries are powerful tools for identifying novel genes implicated in the pathogenesis of obesity and type 2 diabetes.

Adipose Tissue↗