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At least 667 records · Page 37Linked to original sources
PubMed2006

Insulin resistance and low sympathetic nerve activity in the Tsumura Suzuki obese diabetic mouse: a new model of spontaneous type 2 diabetes mellitus and obesity.

Tsumura Suzuki obese diabetic (TSOD) mouse is a new model of type 2 diabetes mellitus and obesity. The TSOD mice had hypoadiponectinemia. To assess the glucose utilization and insulin sensitivity, we examined the effect of insulin (1U/kg) on peripheral tissue glucose uptake in vivo in the TSOD and Tsumura Suzuki nonobese mouse using 2-deoxy-d-[(3)H]glucose. The rates constant of glucose uptake in basal condition without insulin were similar in the peripheral tissues in both strains. Insulin-stimulated glucose uptake by skeletal muscles and adipose tissues in vivo was diminished in the TSOD mice. In addition, we assessed norepinephrine turnover in brown adipose tissue and adrenal epinephrine (E) content and E turnover because disturbances in the sympathetic activities relate to many features in obese and diabetic syndrome. In these mice, the rate of norepinephrine turnover was decreased, and adrenal E content was at most one half of the Tsumura Suzuki nonobese mice and E turnover had extremely low rates. The TSOD mice showed hypercorticosteronemia. These results suggest that TSOD mice have insulin resistance and both low sympathetic nervous activities and low adrenomedullary activity, and have high adrenocortical activity, which are significant features of the TSOD mouse.

Adiponectin↗
PubMed2003

Treatment of obesity: an update on anti-obesity medications.

The information presented in this article provides an overview of physiological agents, therapeutics in current use, and medications that have been extensively used in the past but are no longer available, or are not classically considered as anti-obesity drugs. The authors present an extensive review on the criteria for anti-obesity management efficacy, on physiological mechanisms that regulate central and/or peripheral action energetic homeostasis (nutrients, monoamines and peptides), and on beta-phenethylamine pharmacological-derivative agents (fenfluramine, dexfenfluramine, phentermine, diethylpropion, fenproporex and sibutramine), tricyclic derivatives (mazindol), phenylpropanolamine derivatives (ephedrine, phenylpropanolamine), a phenylpropanolamine oxy-tri-fluor-phenyl derivative (fluoxetine), a naftilamine derivative (sertraline) and a lipstatine derivative (orlistat). An analysis of all clinical trials longer than 10 weeks in duration is also presented for medications used in the management of obesity.

Anti-Obesity Agents↗
PubMed2003

A licorice ethanolic extract with peroxisome proliferator-activated receptor-gamma ligand-binding activity affects diabetes in KK-Ay mice, abdominal obesity in diet-induced obese C57BL mice and hypertension in spontaneously hypertensive rats.

The metabolic syndrome, including type 2 diabetes, insulin resistance, obesity/abdominal obesity, hypertension and dyslipidemia, is a major public health problem. Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) ligands such as thiazolidinediones are effective against this syndrome. In this study, we showed that nonaqueous fractions of licorice (Glycyrrhiza uralensis Fisher) extracted with ethanol, ethyl acetate and acetone, but not an aqueous extract, had PPAR-gamma ligand-binding activity with a GAL4-PPAR-gamma chimera assay. Some prenylflavonoids including glycycoumarin, glycyrin, dehydroglyasperin C and dehydroglyasperin D, a newly found compound, were identified as active compounds with PPAR-gamma ligand-binding activity in the nonaqueous fraction of licorice. A licorice ethanolic extract contained these four active compounds at a total concentration of 16.7 g/100 g extract. Feeding the licorice ethanolic extract at 0.1-0.3 g/100 g diet [approximately 100 to 300 mg/(kg body x d)] for 4 wk decreased (P < 0.05) blood glucose level in younger (6 wk old) and older (13 wk old) diabetic KK-Ay mice and reduced (P < 0.05) weights of intra-abdominal adipose tissues in high fat diet-induced obese C57BL mice. An increase in blood pressure in spontaneously hypertensive rats was suppressed (P < 0.01) by 3 wk of oral administration of the licorice ethanolic extract at 300 mg/(kg body x d). These findings indicate that licorice ethanolic extract is effective in preventing and ameliorating diabetes, ameliorating abdominal obesity and preventing hypertension, and suggest that licorice ethanolic extract would be effective in preventing and/or ameliorating the metabolic syndrome.

Acetates↗
PubMed2005

Pharmacogenetics and obesity: common gene variants influence weight loss response of the norepinephrine/dopamine transporter inhibitor GW320659 in obese subjects.

BACKGROUND: GW320659, a highly selective neuronal norepinephrine and dopamine re-uptake inhibitor, has been evaluated for the treatment of obesity. Scrutiny of the weight loss data from a phase II study (GlaxoSmithKline study OBS20001) showed a wide variation in weight loss response following GW320659 treatment and the possibility that the study population might include subgroups with enhanced weight loss response. METHODS: Pharmacogenetic analysis was performed in 191 subjects prospectively ascertained from a Phase II dose ranging study to evaluate the influence of genotype on weight loss efficacy and safety of GW320659 in obese subjects. RESULTS: Common genetic polymorphisms in the drug target (norepinephrine transporter protein 1, SLC6A2) and mechanism pathway (NMDA receptor channel NR1 subunit, GRIN1) were associated with increased weight loss following GW320659 treatment in a proportion (36%) of the study population. In the patient subgroup selected for these genotypes, GW320659 (15 mg/day) produced a significant difference in mean weight loss of 7.84 kg (SD 5.23, n = 14), compared to 2.53 kg (SD 5.17, n = 24) in the subgroup that did not possess the genotypes (P = 0.006). This subgroup also showed a highly significant weight loss response for GW320659 compared to placebo (+0.31 kg, SD 3.32, n = 16) with the same genotypes (P < 0.0001). In addition, there was no difference in placebo response between either subgroup. CONCLUSIONS: Polymorphisms in SLC6A2 and GRIN1 could be used to maximize effective obesity pharmacotherapy by norepinephrine/dopamine transporter inhibitors by identifying patients that may be predisposed to particularly good treatment weight loss response.

Administration, Oral↗
PubMed2006

Impact of spinal anaesthesia on peri-operative lung volumes in obese and morbidly obese female patients.

Although obesity predisposes to postoperative pulmonary complications, data on the relationship between body mass index (BMI) and peri-operative respiratory performance are limited. We prospectively studied the impact of spinal anaesthesia, obesity and vaginal surgery on lung volumes measured by spirometry in 28 patients with BMI 30-40 kg.m(-2) and in 13 patients with BMI > or = 40 kg.m(-2). Vital capacity, forced vital capacity, forced expiratory volume in 1 s, mid-expiratory and peak expiratory flows were measured during the pre-operative visit (baseline), after effective spinal anaesthesia with premedication, and after the operation at 20 min, 1 h, 2 h, and 3 h (after mobilisation). Spinal anaesthesia and premedication were associated with a significant decrease in spirometric parameters. Spinal anaesthesia and premedication were associated with a significant decrease in spirometric parameters; mean (SD) vital capacities were - 19% (6.4) in patients with BMI 30-40 kg.m(-2) and - 33% (9.0) in patients with BMI > 40 kg.m(-2). The decrease of lung volumes remained constant for 2 h, whereas 3 h after the operation and after mobilisation, spirometric parameters significantly improved in all patients. This study showed that both spinal anaesthesia and obesity significantly impaired peri-operative respiratory function.

Adult↗
PubMed2001

Detection and identification of subcutaneous adipose tissue protein related to obesity in New Zealand obese mouse.

New Zealand obese (NZO) mouse, a genetic model of obesity, shows hyperphagia, hyperinsulinemia and leptin resistance. We analyzed subcutaneous adipose tissue proteins in NZO mice with a two-dimensional gel electrophoresis technique followed by protein sequence analysis. NZO mice showed hyperinsulinemia and hyperleptinemia. Abdominal subcutaneous adipose tissue was inspected in NZO and C57BL/6J lean mice. Two-dimensional gel electrophoresis detected 4 spots which were obviously reduced in NZO mice. Those spots were p26, p19, p18 and p15. Internal sequences of the p26 and p15 protein were homologous with those of carbonic anhydrase III, p19 was cytochrome b5, p18 was superoxide dismutase. Serum arachidonic acid level in NZO mice was lower by 80% of C57BL/6J mice. The present study demonstrated the reduction of several enzymes related to lipid metabolism in NZO mice. These data raises the hypothesis that the supposed changes of membrane fluidity caused by altered membrane lipid content may involve central leptin resistance of this model of obesity.

Adipose Tissue↗
PubMed1990

Mitigation of obesity by BRL 26830A, a new beta-adrenoceptor agonist, in MSG obese mice.

Half of the mice in both the monosodium-L-glutamate (MSG)-induced obesity and saline control groups were given BRL 26830A via a gastric tube at a daily dose of 5 mg/kg for 2 weeks, and the other half given distilled water. BRL 26830A administration significantly increased guanosine-5'-diphosphate (GDP)-binding in brown adipose tissue (BAT) and the resting metabolic rate (RMR), and significantly reduced retroperitoneal white adipose tissue (WAT) pads in both groups. It also markedly reduced body weight in MSG obese mice that had reduced BAT thermogenesis and decreased RMR. However, food intake was unchanged in both groups. Neither beta 1- nor beta 2-selective antagonists affected the increase of RMR induced by BRL 26830A, but a non-selective beta-antagonist completely inhibited its increase. These results suggest that BRL 26830A, which is a new beta-adrenoceptor agonist, stimulates BAT thermogenesis, increases RMR, and reduces WAT, thus contributing to the mitigation of obesity.

Adipose Tissue↗
PubMed1996

Adrenalectomy reverses pre-existing obesity in adult genetically obese (ob/ob) mice.

OBJECTIVE: To determine if adrenalectomy would reverse the pre-existing gross obesity, characteristic of adult genetically obese (ob/ob) mice. DESIGN: Adult (12 week old) female ob/ob mice were adrenalectomized and fed a stock diet for 6 or 14 weeks. They were housed at 23-25 degrees C or 33 degrees C. Food intake and total body energy were determined. RESULTS: Adrenalectomy abolished the hyperphagia characteristic of ob/ob mice. Adrenalectomized ob/ob mice consumed 8-17% less food than intact lean mice. Adrenalectomized ob/ob mice housed at 23-25 degrees C lost 55% of their pre-existing body energy within 6 weeks after surgery and 75% of their body energy within 14 weeks after surgery. At 14 weeks after surgery, body weights and body energy content of the adrenalectomized ob/ob mice were comparable with values for intact lean mice. Intact ob/ob mice pair-fed to adrenalectomized ob/ob mice lost only half as much body energy as the adrenalectomized ob/ob mice did, indicating that adrenalectomy not only diminished food intake in ob/ob mice but also increased their energy expenditure per unit food consumed. Adrenalectomized ob/ob mice housed at 33 degrees C lost only half as much body energy in 6 weeks as did mice housed at 23-25 degrees C. CONCLUSION: Adrenalectomy reverses the gross obesity characteristic of adult ob/ob mice by abolishing their hyperphagia and increasing their energy expenditure per unit food consumed.

Adrenalectomy↗
PubMed1990

Growth in obese children treated for obesity.

This study assesses the growth patterns during a 5-year period in children aged 6 to 12 years treated for obesity using behavioral family-based treatment procedures. Previous studies have suggested a decrease in height velocity after weight reduction, but these results did not consider either the height of the parent or the greater height of obese than nonobese children. Results show that at entry, obese children are taller than their nonobese peers (74th percentile), and that even after 5 years, they remain taller than the norm (65th percentile). Child weight and level of physical maturity accounted for 54% of the variance in predicting baseline height percentile. Entrance height and parental height accounted for 9% of the variance in changes in height percentile, both adjusted for parental height. Weight change did not correlate with growth adjusted for parental height. These results do not suggest that negative effects on height are a long-term side effect of child weight control.

Behavior Therapy↗
PubMed1977

Behavioral treatment of obesity. Limitations and results with the chronically obese.

Results of behavioral treatment for obese persons during the first 18 months of clinical operation are presented and other reports in the literature are reviewed. Baseline and follow-up data were gathered from a population of 144 female, chronically obese patients, most of whom were experiencing medical complications associated with obesity. Treatment results were disappointing in comparison with results of similar programs. Difference in patient population groups is offered as a possible explanation for this phenomenon. Covariant analyses of demographic and psychosocial variables failed to yield any clear predictors of weight loss; it is suggested that biological factors may be important to treatment outcome for some overweight patients.

Behavior Therapy↗
PubMed1994

Eating disorder inventory in the assessment of psychosocial status in the obese patients prior to and at long-term following biliopancreatic diversion for obesity.

Psychological traits of obese patients, assessed with the Eating Disorder Inventory (EDI), were compared to those of subjects in the long-term following biliopancreatic diversion for obesity (BPD), when body weight has been steadily normal for over 1 year and any preoccupation with dieting and weight has been completely abandoned. The overall results suggest that the stable body weight normalization on a completely free diet does confer considerable psychological benefit on obese individuals. On the basis of the EDI results, post-BPD subjects were divided into weight-preoccupied and not-weight-preoccupied individuals. In the not-weight-preoccupied subjects, the psychosocial status and emotional rectivity were closely similar to those observed in lean control persons, whereas the few weight-preoccupied subjects, in spite of completely normal body weight, showed residual body dissatisfaction and personality traits very similar to those of eating-disordered patients.

Adolescent↗
PubMed2000

Genetic evidence for obesity loci involved in the regulation of body fat distribution in obese type 2 diabetes rat, OLETF.

The Otsuka Long-Evans Tokushima Fatty (OLETF) rat is an animal model for obese type 2 diabetes in human. Obesity is essential for the onset of type 2 diabetes in this rat. Our present investigation was designed to identify quantitative trait loci (QTLs) contributing to obesity by performing a whole-genome search using 214 F(2) intercross progeny between OLETF and F344 rats. We have identified six QTLs responsible for adiposity indices of fat pads on rat chromosomes 2 (Obs1 for mesenteric fat), 4 (Obs2 for retroperitoneal fat), 8 (Obs3 for mesenteric fat), 9 (Obs4 for retroperitoneal fat), and 14 (Obs5 and Obs6 for retroperitoneal fat), demonstrating that the adiposity indices of individual fat pads were under the control of different genes. As expected, the OLETF allele corresponds to increased adiposity indices for all QTLs, except for Obs3, in which the F344 allele leads to an increase in the index.

Adipose Tissue↗
PubMed2000

Birth weight and the insulin resistance syndrome: association of low birth weight with truncal obesity and raised plasminogen activator inhibitor-1 but not with abdominal obesity or plasma lipid disturbances.

AIMS/HYPOTHESIS: To distinguish the physiological disturbances related to birth weight from the cluster of disturbances called the insulin resistance syndrome. METHODS: Men participating in a population-based study in Uppsala, Sweden, with recordings of birth weight, were metabolically characterised at age 50 (n = 1268) and re-investigated at age 70 (n = 734). Blood pressure, BMI, glucose and insulin concentrations are associated with birth weight in this cohort. RESULTS: Birth weight was inversely associated (p < 0.03) with subscapular:triceps skinfold ratio (truncal fat), plasminogen activator inhibitor-1 (PAI-1) activity, specific insulin and proinsulin-like molecules when adjusted for BMI. Birth weight was not related (p > 0.10) with waist circumference, serum triglycerides or HDL cholesterol. The insulin resistance syndrome was defined as the combination of hypertension, insulin resistance and dyslipidaemia. The prevalence of this syndrome at age 50 and 70 was inversely related to birth weight with odds ratio 0.66 and 0.71, respectively, per kg increase in birth weight. When the syndrome was defined to include truncal obesity or raised plasminogen activator inhibitor-1 instead of dyslipidaemia, the corresponding odds ratios were 0.51 and 0.66, respectively. CONCLUSIONS/INTERPRETATION: Low birth weight predicts high blood pressure, insulin resistance, truncal obesity and high plasminogen activator inhibitor-1 activity but not the abdominal obesity or dyslipidaemia present in the insulin resistance syndrome. The cluster of disturbances associated with low birth weight is a subset of the disturbances that are clustered in the general population as the insulin resistance syndrome. This subset of physiological disturbances is possibly linked by a specific pathway.

Aged↗
PubMed1991

Reduced hypothalamic neurotensin concentrations in the genetically obese diabetic (ob/ob) mouse: possible relationship to obesity.

Hypothalamic tissue levels of nine regulatory peptides (bombesin, calcitonin gene-related peptide [CGRP], galanin, neuromedin B, neuropeptide Y [NPY], neurotensin, somatostatin, substance P, and vasoactive intestinal peptide [VIP]) were compared in Aston obese diabetic (ob/ob) and lean (+/?) mice aged 4, 16, and 28 weeks. Neurotensin concentrations were significantly lower in ob/ob mice than in lean mice, with a 20% reduction (P = .03) in the whole hypothalamus at 4 weeks of age, a 24% reduction (P = .009) in the lateral hypothalamus at 16 weeks, and a 50% reduction (P = .0007) in the central hypothalamus at 28 weeks of age. Apart from a 42% increase in vasoactive intestinal peptide concentrations in the central hypothalamus of ob/ob mice at 28 weeks (P = .02), levels of the other eight peptides examined did not differ significantly between obese and lean groups. Neurotensin is known to cause anorexia and increased energy expenditure when injected into the central hypothalamus. Reduced hypothalamic neurotensin concentrations may reflect reduced neurotensinergic activity, which might contribute to hyperphagia and decreased energy expenditure, two major defects that contribute to obesity and diabetes in the ob/ob syndrome.

Analysis of Variance↗
PubMed2006

Effects of abdominal electroacupuncture on parameters related to obesity in obese women: a pilot study.

The aim of this study was to elucidate the effects of electroacupuncture at abdominal meridian points on various obesity-related parameters: body weight (BW), body fat (BF) percentage, body mass index (BMI), percent ideal body weight (PIBW), and waist (WC) and hip (HC) circumferences. All of these parameters changed significantly compared to pretreatment in this pilot uncontrolled study involving 31 women with obesity. The percent reductions were 5.3% in BW, 1.3% in BF, 4.7% in BMI, 6.0% in PIBW, 4.6% in WC, 6.2% in HC, and 2.1% in the WC/HC ratio. The most affected variable was WC (effect size=0.58). Since this was a pilot study with several limitations, such as a small sample size and absence of a control treatment and appropriate follow-up, further studies that include a randomized design, larger sample sizes, and more detailed data about the subjects are needed to convincingly show the effects of electroacupuncture at abdominal meridian points on overweight and obese patients.

Adipose Tissue↗
PubMed2005

Adipocyte insensitivity syndromes -- novel approach to nutritional metabolic problems including obesity and obesity related disorders.

Progresses in molecular biology have highlighted the central role of adipocytes in the development of obesity and other nutrition based disorders. Adipocytes, by virtue of their excellent and sensitive molecular machinery, seem to reflect nutritional alterations very precisely. Adipocyte determination and differentiation factor 1 (ADD1)/sterol regulatory element binding protein-1c (SREBP-1c), which is the main transcription factor, regulates the characteristic features of adipocyte, senses the glucose and fat excess and draws the excess into the adipocyte to preserve energy, and maintains the blood biochemistry within physiological ranges. ADD1/SREBP-1c has regulatory functions via transactivation over the other important mature adipocyte markers such as leptin, peroxisome proliferator-activated receptor gamma (PPARgamma) and lipogenic enzymes. In this paper, considering to the role of ADD1/SREBP-1c on adipogenic markers, two new concepts have been defined: the first is sensitive adipocyte, implying a fat cell that functions perfectly at molecular level; and the second is adipocyte insensitivity syndrome (AIS), in which deviations from the optimal function of adipocyte leads to various metabolic abnormalities. The two extreme ends for adipocyte function; obesity and lipodystrophy, and intermediate spectrums between these are categorized into four subgroups. According to this categorization, responses of adipogenic markers to the stimulation of the master transcription factor, ADD1/SREBP-1c might be different in adipocytes: higher lipogenic enzymes activities in type I AIS, insufficient transactivation of leptin in type II AIS, failure in the expression of PPARgamma in type III AIS, and insufficient increases of lipogenic enzymes in type IV AIS. The novel AIS classification, which asserts that the adipocyte has a central importance for the development of metabolic devastating diseases like obesity, metabolic syndrome, type 2 diabetes and atherosclerosis, provides simpler but effective answers for the puzzle by unifying the recent, good quality studies and points out to new therapeutic approaches, highlighting the possible molecular defects.

Adipocytes↗
PubMed2005

An alternative hypothesis to the obesity epidemic: obesity is due to increased maternal body size, birth size, growth rate, and height.

A new hypothesis for dealing with the obesity epidemic is based on changing several factors normally considered desirable by the medical community. These factors include reductions in pre-pregnancy maternal weight, modest reduction of infant birthweight, slower childhood and adolescent growth and reduced caloric intake from infancy through adulthood. The underlining roots for the obesity epidemic involve raised levels of insulin, insulin-like growth factor-1 and cell proliferation which are subject to human control. The implication of this hypothesis is that current measures are inadequate unless a much more comprehensive response is implemented to deal with the obesity epidemic.

Birth Weight↗