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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To estimate the renal glucose threshold, we measured glucosuria in 546 oral glucose tolerance tests (OGTT) (glucose oxidase method). The subjects, with normal renal function, presented during OGTT one or several peak plasma glucose levels between 10 and 13.4 mmol/l. The renal glucose threshold was thus higher than 10 mmol/l in the 43% of this population who were a glucosuric (normal renal threshold was between 8.8 and 10 mmol/l). The frequency of raised threshold was higher in obese patients than in subjects of normal body weight: indeed from 34% in non obese patients rates rose respectively at 37%, 50% and 68% in obesity groups (10 to 30%, 30 to 50% and 50% over ideal body weight (respectively). This trend was found regardless of the type of glucose tolerance response (ie. normal, IGT, non diagnostic, NIDD).
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PMID:[Effect of obesity on the elevation of renal glucose threshold. Studies during oral glucose tolerance tests (author's transl)]. 709 42

A total of 1,011 clinically asymptomatic adults older than 20 years of age, with a minimal fasting of one hour, were screened for diabetes mellitus. This group was selected from a community medical service. The presence of diabetes in first degree relatives (parents, brothers/sisters and children) was investigated by interrogation of the subjects. Weight, height, and the waist and hip perimeters were measured, and the body mass index and the waist/hip ratio were calculated. Obesity was present in 26% of the population and 35.6% had a relative with diabetes mellitus, but 53.8% were younger than 40 years. A capillary blood sample was taken and glucose was measured by a reflectometer glucometer. Individuals with blood glucose levels of 160 mg/dL or higher were appointed for a fasting venous blood sample and glucose was analyzed using the glucose oxidase method. If the glucose levels were > 140 mg/dL, a second fasting venous blood sample was taken 1-2 weeks later, if both results were > 140 mg/dL a diagnosis of diabetes mellitus was established; otherwise it was considered non diagnostic for diabetes mellitus. A total of 17 were detected with > 160 mg/dL by the glucometer and 12/17 persons were diagnosed with diabetes mellitus (1.2%). No person younger than 30 years was detected (n = 307), but 3/237 were detected in the thirty years group (1.26% for this group) and 9 persons were older than 40 years, 1.2% of the total group. Capillary glucose measurements may be used for screening of populations selecting those who require to be submitted to diagnostic tests.
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PMID:[Detection of non-insulin-dependent diabetes mellitus in asymptomatic adults]. 815 75

The relationship between insulinaemia and obesity and glucose tolerance and the impact of pregnancy as risk factor for carbohydrate abnormalities were investigated in 91 consecutive patients with polycystic ovary syndrome (PCOS) aged 26-32 years. Fifteen normoglycaemic patients became pregnant within 6 months of the pregestational study using pharmacological induction of ovulation. Plasma concentrations of insulin and glucose after an oral glucose tolerance test (OGTT) were determined by immunoradiometric assay and glucose oxidase technique respectively. OGTT patients were classified according to their response as normoinsulinaemic (n = 46) or hyperinsulinaemic (n = 45). Impairment of glucose metabolism occurred in 12.1% (n = 11, 10 obese and one lean) of all PCOS subjects. Based on insulin secretion, 6.5% of normoinsulinaemic and 13.3% of hyperinsulinaemic patients had an impaired glucose tolerance and 2.3 and 2.2% respectively a non-insulin-dependent diabetes mellitus. Obese patients had higher values for area under the curve for insulin response to OGTT (I-AUC values) than lean patients, and the percentage above ideal body weight was greater in hyperinsulinaemic than in normoinsulinaemic patients. All hyperinsulinaemic (7/15) subjects who became pregnant developed an impairment of glucose metabolism during pregnancy. It is concluded that the PCOS population was at higher risk of developing carbohydrate abnormalities than the normal population of a similar reproductive age. Furthermore, those with abnormal insulin secretion at the pregestational stage may, during pregnancy, develop an impaired gestational glucose tolerance or gestational diabetes.
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PMID:Preconceptional and gestational evaluation of insulin secretion in patients with polycystic ovary syndrome. 898 Nov 15

Obesity has been mentioned as a major risk factor to develop gestational diabetes mellitus (GDM). In this work the main purpose was to compare the distribution of body fat tissue and insulin serum levels in obese women suffering GDM. Twenty obese pregnant patients, ten with GDM and ten non-diabetic control subjects were selected. To define the body fat distribution the following anthropometric indexes were performed: subscapular/triceps skinfold index (STI) during pregnancy (24-28 weeks) and STI plus waist/hip ratio (WHR) in postpartum (6 weeks). The two obese groups were evaluated through an oral glucose tolerance test, taking blood at 0, 60, 120 and 180 minutes; after centrifugation glucose serum levels were measured immediately by the glucose oxidase technique and the rest of the sample was kept frozen at -20 degrees C until insulin determinations by radioimmunoassay. The ten patients with GDM presented upper body fat, segment distribution, while among those without GDM, only six had this last feature and four were found with lower body fat segment distribution (p < 0.047). Insulin serum levels in GDM group were higher than in women without GDM (p < 0.01). The STI during and after pregnancy correlated positively (r = 0.77, p < 0.00003) and also with WHR (r = 0.61, p < 0.0001). There was correlation between STI and WHR both measured in postpartum (r = 0.52, p < 0.0007).
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PMID:[Distribution of adipose tissue and insulin serum levels in women with gestational diabetes]. 1054 41

Obesity is an increasing nutritional disorder in developed countries, and oxidative stress has been identified as a key factor in numerous pathologies such as diabetes, inflammation, and atherosclerosis, which are favored by obesity. The objective of the present study was to investigate the effects of oxidative stress in 3T3-L1 adipose cells on two parameters involved in metabolic complications associated with obesity, namely adiponectin secretion and lactate production. Differentiated 3T3-L1 adipose cells were exposed to increasing concentrations of glucose oxidase. 4-Hydroxynonenal (4-HNE), a relevant lipid peroxidation by-product which may affect several metabolic processes in making covalent adducts with various molecules; adiponectin secretion; and lactate production were measured in response to glucose oxidase exposure. Results show an inhibition of adiponectin mRNA expression by glucose oxidase and a significant inverse correlation between 4-HNE formation and adiponectin secretion. Furthermore, 4-HNE alone inhibits adiponectin production by 3T3-L1. On the other hand, glucose oxidase and 4-HNE significantly stimulated lactate production by 3T3-L1 adipocytes. These results demonstrate that adipose cells are highly sensitive to oxidative stress, with subsequent decreased adiponectin secretion and increased lactate production, two events involved in the development of insulin resistance.
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PMID:Effects of oxidative stress on adiponectin secretion and lactate production in 3T3-L1 adipocytes. 1574 84

Obesity is increasing all over the world, its morbidity justifying a serious effort to improve the situation. Diet and physical exercise constitute major measures to fight obesity. We aimed to investigate the effect of acute exercise intensity over plasma insulin, growth hormone and somatostatin responses. Plasma levels of insulin, growth hormone, somatostatin and glucose were measured at baseline, after 15 minutes of moderate intensity exercise and after 15 minutes of high intensity exercise in a group of young healthy volunteers. Insulin, growth hormone and somatostatin were measured by immunoradioassay and glucose by a glucose oxidase method. After moderate intensity exercise plasma insulin levels tended to decrease, growth hormone tended to increase and somatostatin did not change. A similar period of high intensity exercise led to a similar decrease of plasma insulin, a much higher increase of growth hormone plasma level and no change of somatostatin. Glycemia suffered no significant change throughout the experiment. We conclude that hormonal changes induced by physical exercise depend on the intensity of exercise. When comparing moderate with high intensity exercise, a similar response of plasma insulin and a lower growth hormone/somatostatin ratio may support a healthier cardiovascular effect for moderate intensity exercise.
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PMID:[Impact of acute exercise intensity on plasma concentrations of insulin, growth hormone and somatostatin]. 1592 47

Increased oxidative stress has been associated with obesity-related disorders. In this study, we investigated how oxidative stress, in different ways of exposure, regulates gene expression of various adipokines in 3T3-L1 adipocytes. Exposure to 100-500microM H(2)O(2) for 10min, as well as exposure to 5-25mU/ml glucose oxidase for 18h, similarly decreased adiponectin, leptin, and resistin mRNAs, and increased plasminogen activator inhibitor-1 mRNA. Secretion levels of adipokines were also changed by oxidative stress in parallel with mRNA expression levels. Although a peak increase in plasminogen activator inhibitor-1 mRNA was achieved between 4 and 8h after exposure to H(2)O(2) for 10min, significant decreases in adiponectin and resistin mRNA were observed after 16h, while leptin mRNA was decreased earlier. Our results suggest that oxidative stress, even of short duration, has a significant impact on the regulation of various adipokine gene expressions favoring atherosclerosis.
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PMID:Oxidative stress provokes atherogenic changes in adipokine gene expression in 3T3-L1 adipocytes. 1631 Jan 64

The expression of resistin protein in normal human abdominal, thigh, pregnant women abdominal, non-pregnant women abdominal subcutaneous adipose tissue and placenta and the relationship between obesity, type 2 diabetes mellitus (T2DM), pregnant physiological insulin resistance (IR) and gestational diabetes mellitus (GDM) was investigated. The expression of resistin protein in normal human abdominal, thigh, pregnant women abdominal, non-pregnant women abdominal subcutaneous adipose tissue and placenta was detected by using Western blotting method. Fasting serum glucose concentration was measured by glucose oxidase assay. Serum cholesterol (CHOL), serum triglycerides (TG), serum HDL cholesterol (HDL-C) and serum LDL cholesterol (LDL-C) were determined by full automatic biochemical instrument. Fasting insulin was measured by enzyme immunoassay to calculate insulin resistance index (IRI). Height, weight, systolic blood pressure (SBP) and diastolic blood pressure (DBP) were measured to calculate body mass index (BMI) and body fat percentage (BF %). Resistin protein expression in pregnant women placental tissue (67 905 +/- 8441) (arbitrary A values) was much higher than that in subcutaneous adipose tissue in pregnant women abdomen (40 718 +/- 3818, P < 0.01), non-pregnant women abdomen (38 288 +/- 2084, P < 0.01), normal human abdomen (39 421 +/- 6087, P < 0.01) and thigh (14 942 +/- 6706, P < 0.001) respectively. The resistin expression in abdominal subcutaneous adipose tissue showed no significant difference among pregnant, non-pregnant women and normal human, but much higher than that in thigh subcutaneous adipose tissue (P < 0.001). Pearson analysis revealed that resistin protein was correlated with BMI (r = 0.42), fasting insulin concentration (r = 0.38), IRI (r = 0.34), BF % (r = 0.43) and fasting glucose (r = 0.39), but not with blood pressure, CHOL, TG, HDL-C and LDL-C. It was suggested that resistin protein expression in human abdominal subcutaneous adipose tissue was much higher than that in human thigh subcutaneous adipose tissue. Resistin was closely related with central obesity, leading to IR, subsequently obesity and T2DM. Resistin protein expression in placental tissue was much higher than that in subcutaneous adipose tissue in normal human abdomen, pregnant abdomen, non-pregnant women abdomen and thigh. It was indicated that resistin protein could be secreted from human placental tissue. Resistin might be one of the factors that lead to pregnant physiological IR and GDM.
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PMID:Expression of resistin protein in normal human subcutaneous adipose tissue and pregnant women subcutaneous adipose tissue and placenta. 1696 Dec 71

The release of fatty acids and glycerol from lipid droplets (LD) of mammalian adipose cells is tightly regulated by a number of counterregulatory signals and negative feedback mechanisms. In humans unrestrained lipolysis contributes to the pathogenesis of obesity and type II diabetes. In order to identify novel targets for the pharmacological interference with lipolysis, the molecular mechanisms of four antilipolytic agents were compared in isolated rat adipocytes. Incubation of the adipocytes with insulin, palmitate, glucose oxidase (for the generation of H2O2) and the antidiabetic sulfonylurea drug, glimepiride, reduced adenylyl cyclase-dependent, but not dibutyryl-cAMP-induced lipolysis as well as the translocation of hormone-sensitive lipase and the LD-associated protein, perilipin-A, to and from LD, respectively. The antilipolytic activity of palmitate, H2O2 and glimepiride rather than that of insulin was dependent on rolipram-sensitive but cilostamide-insensitive phosphodiesterase (PDE) but was not associated with detectable downregulation of total cytosolic cAMP and insulin signaling via phosphatidylinositol-3 kinase and protein kinase B. LD from adipocytes treated with palmitate, H2O2 and glimepiride were capable of converting cAMP to adenosine in vitro, which was hardly observed with those from basal cells. Conversion of cAMP to adenosine was blocked by rolipram and the 5'-nucleotidase inhibitor, AMPCP. Immunoblotting analysis revealed a limited salt-sensitive association with LD of some of the PDE isoforms currently known to be expressed in rat adipocytes. In contrast, the cAMP-to-adenosine converting activity was stripped off the LD by bacterial phosphatidylinositol-specific phospholipase C. These findings emphasize the importance of the compartmentalization of cAMP signaling for the regulation of lipolysis in adipocytes, in general, and of the involvement of LD-associated proteins for cAMP degradation, in particular.
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PMID:Inhibition of lipolysis by palmitate, H2O2 and the sulfonylurea drug, glimepiride, in rat adipocytes depends on cAMP degradation by lipid droplets. 1818 16

Circadian rhythmicity is affected in obese subjects. This article analyzes the effect of a high-fat diet (35% fat) on 24-h changes circulating prolactin, luteinizing hormone (LH), testosterone, corticosterone, thyroid-stimulating hormone (TSH) and glucose, and pineal melatonin content, in rats. When body weight of rats reached the values of morbid obesity, the animals were sacrificed at six different time intervals throughout a 24-h cycle, together with age-matched controls fed a normal diet (4% fat). Plasma hormone levels were measured by specific radioimmunoassays and glucose concentration by an automated glucose oxidase method. In rats under a high-fat diet, a significant disruption of the 24-h pattern of plasma TSH, LH, and testosterone and a slight disruption of prolactin rhythm were found. Additionally, high-fat fed rats showed significantly lower total values of plasma TSH and testosterone and absence of correlation between testosterone and circulating LH levels. Plasma corticosterone levels increased significantly in high-fat fed rats and their 24-h variation became blunted. In obese animals, a significant hyperglycemia developed, individual plasma glucose values correlating with circulating corticosterone in high-fat fed rats only. The amplitude of the nocturnal pineal melatonin peak decreased significantly in high-fat fed rats. The results underlie the significant effects that obesity has on circadian organization of hormone secretion.
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PMID:Effect of a high-fat diet on 24-h pattern of circulating levels of prolactin, luteinizing hormone, testosterone, corticosterone, thyroid-stimulating hormone and glucose, and pineal melatonin content, in rats. 1844 10


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