Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous cross-sectional studies show that puberty is associated with a reduction in insulin sensitivity (S(I)), but no longitudinal studies have examined this change in detail. This study is a longitudinal study in 60 children (33 male and 27 female subjects; 32 Caucasian and 28 African-American) examined at Tanner stage I (age 9.2 +/- 1.4 years) and after 2.0 +/- 0.6 years of follow-up, by which time 29 children remained at Tanner stage I and 31 had progressed to Tanner stage III or IV. Tanner stage was assessed by physical examination. S(I), the acute insulin response (AIR), and the disposition index (DI) were determined by the tolbutamide-modified intravenous glucose tolerance test and minimal modeling, body fat mass was assessed by dual-energy X-ray absorptiometry, visceral fat was determined by computed tomography, and fasting blood was analyzed for hormone levels. In children progressing to Tanner stage III, S(I) fell significantly by 32% (4.4 +/- 3.0 to 3.0 +/- 1.7 x 10(-4)min(-1)/[microIU/ml]), AIR increased by 30%, DI fell by 27%, and there was a significant increase in fasting glucose (93.5 +/- 5.0 to 97.0 +/- 4.1 mg/dl) and insulin (14.3 +/- 8.1 to 18.6 +/- 11.0 microIU/ml). In children remaining at Tanner stage I, there was a slight increase in S(I) (6.4 +/- 3.1 to 7.4 +/- 3.5 x 10(-4)min(-1)/[microIU/ml]) with no significant change in AIR or fasting glucose and insulin. The pubertal fall in S(I) was more consistent in African-Americans; remained significant after controlling for age, sex, and change in fat mass, visceral fat, and fat-free mass; and was similar in children at low, medium, and high body fat. Change in S(I) was not significantly related to change in fasting hormone levels, but change in AIR was significantly related to change in androstendione (r = 0.39; P = 0.04). Pubertal transition from Tanner stage I to Tanner stage III was associated with a 32% reduction in S(I,) and increases in fasting glucose, insulin, and AIR. These changes were similar across sex, ethnicity, and obesity. The significant fall in DI suggests conservation in beta-cell function or an inadequate beta-cell response to the fall in S(I). The fall in S(I) was not associated with changes in body fat, visceral fat, IGF-I, androgens, or estradiol.
 ...
PMID:Longitudinal study on pubertal insulin resistance. 1167 20

Studies on the role of parental history on the risk of developing metabolic syndrome (MS) show inconsistent data that may depend on misclassification of the parental history. Confirming carefully the parental phenotype (PF) of type 2 diabetes mellitus (DM) and essential hypertension (EH) of participants' parents, we determined the relationship between PF of either DM or EH and the risk of developing MS in Mexican individuals. A case-control study of 210 subjects randomly recruited from Durango, Mexico was carried out. Subjects with MS (cases) were compared with a control group of subjects without MS matched by age and gender. MS was defined by the presence of two or more of the following: fasting glucose > or =7.0 mmol/l; blood pressure > or =160/90 mmHg; fasting triglycerides > or =1.7 mmol/l and/or HDL-cholesterol <1.0 mmol/l; and obesity (body mass index > or =30 kg/m2 and/or waist-to-hip ratio > or =0.85). The PF of DM and EH was confirmed by direct clinical examination and/or review of certificates of death of each of the participants' parents. Incomplete or unclear data about PH were exclusion criteria. Multivariate analysis showed that PF of DM without EH (odds ratio (OR) 2.6; 95% CI, 1.3-7.8, p=0.044) and PF of both DM and EH (OR, 3.1; 95% CI, 1.5-9.1, p=0.0001), but not the PF of EH without DM are independent predictors for developing MS in Mexican individuals. In the offspring generation of Mexican subjects, the PF of DM seems to increase the risk of developing MS, whereas PF of EH does not.
Acta Diabetol 2001
PMID:The parental phenotype of diabetes, but not of essential hypertension, is linked to the development of metabolic syndrome in Mexican individuals. 1175 7

The aim of the study was to determine the influence of adiposity on the relationship between bioelectrical impedance (BIA) measurements of body segments and estimation of body composition by dual-energy X-ray absorptiometry (DXA). Multiple frequencies of whole body and segmental impedances were measured in 68 normal-weight and obese subjects (46 women and 22 men), mean age 37.2+/-14.8 years (range, 18-69). Total and appendicular lean body mass (LBM) assessed by DXA correlated significantly with total and segmental impedance values adjusted for stature in both obese and normal-weight subjects. Best fitting equations for the prediction of appendicular LBM from segmental impedance measurements were derived for the arm and leg with and without the inclusion of adiposity (the percentage of body fat measured by DXA) in the regression models. Best prediction was obtained at low frequency for the arm and high frequency for the leg. Adiposity appears to significantly influence the prediction of leg LBM by BIA. These preliminary observations need further validation to provide an accurate assessment of appendicular LBM assessment by BIA.
Acta Diabetol 2001
PMID:Prediction of lean body mass from multifrequency segmental impedance: influence of adiposity. 1175 8

We evaluated the possible additive effect of overweight and diabetes in the occurrence of coronary heart disease (CHD) and stroke, and their interaction with other established risk factors. In a cross-sectional study, we evaluated the frequency of CHD and stroke in four groups of subjects: (1) lean non-diabetic subjects (n=250); (2) lean diabetic subjects (n=269); (3) overweight non-diabetic subjects (n=203); and (4) overweight diabetic subjects (n=446). CHD was more frequent among diabetic subjects, and even more among overweight diabetic subjects; stroke was more frequent among diabetic subjects, but equally frequent in overweight and in lean diabetic subjects. At multiple logistic regression analysis, age, arterial hypertension, diabetes were independent risk factors for CHD and for stroke; BMI and hyperlipidemia were risk factors only for CHD. CHD was an independent risk factor for stroke, and stroke was a risk factor for CHD. We conclude that obesity and diabetes are additional risk factors for CHD but not for stroke. The value of established risk factors such as arterial hypertension and hyperlipidemia in determining the appearance of CHD and stroke is maintained in the presence overweight and diabetes. Finally, CHD is frequently associated with stroke, suggesting a common process of atherosclerosis underlying both diseases.
Acta Diabetol 2002 Jun
PMID:Additive effect of overweight and type 2 diabetes in the appearance of coronary heart disease but not of stroke: a cross-sectional study. 1212 Sep 18

Low serum magnesium levels are related to diabetes mellitus (DM) and high blood pressure (HBP), but as far as we know, there are no previous reports that analyzed the serum magnesium concentration in individuals with metabolic syndrome (MS). We performed a cross-sectional population-based study to compare 192 individuals with MS and 384 disorder-free control subjects, matched by age and gender. Magnesium supplementation treatment and conditions likely to provoke hypomagnesemia, including previous diagnosis of diabetes mellitus (DM) and/or high blood pressure (HBP), were exclusion criteria. In this regard, only incident cases of DM and HBP were included. MS was defined by the presence at least of two of the following features: hyperglycemia (> or =7.0 mmol/l); HBP (> or =160/90 mmHg); dyslipidemia (fasting triglycerides > or =1.7 mmol/l and/or HDL-cholesterol <1.0 mmol/l); and obesity (body mass index > or =30 kg/m(2) and/or waist-to-hip ratio > or =0.85 in women or > or =0.9 in men). Low serum magnesium levels were identified in 126 (65.6%) and 19 (4.9%) individuals with and without MS, p<0.00001. The mean serum magnesium level among subjects with MS was 1.8+/-0.3 mg/dl, and among control subjects 2.2+/-0.2 mg/dl, p<0.00001. There was a strong independent relationship between low serum magnesium levels and MS (odds ratio (OR)=6.8, CI(95%) 4.2-10.9). Among the components of MS, dyslipidemia (OR 2.8, CI(95%) 1.3-2.9) and HBP (OR 1.9, CI(95%) 1.4-2.8) were strongly related to low serum magnesium levels. This study reveals a strong relationship between decreased serum magnesium and MS.
Acta Diabetol 2002 Dec
PMID:Low serum magnesium levels and metabolic syndrome. 1248 95

Galanin, a 29-30 amino-acid neuropeptide is distributed in the central and peripheral nervous systems, the pituitary gland, the gastrointestinal tract and also in the pancreas. The endogenous and exogenous effects of galanin are mediated by three receptor subtypes, which are termed: GALR1, GALR2, and GALR3. Galanin has a significant role in physiological and pathological processes in adults as well as in children. It has an ability to contract smooth muscles in GI (facilitation and inhibition), stimulates reflexes in the CNS, decreases pancreatic amylase secretion, changes transport of electrolytes Na+ and CL-. It takes part in etiopathogenesis of depression, Alzheimer's disease and diarrhoea, exerts tonic inhibition of nociceptive input to the central nervous system and regulates a function of hypothalamic-pituitary system. Galanin decreases insulin and somatostatin secretion, increases glucagon secretion, takes part in prolactin release, stimulates growth hormone-releasing hormone, hypothalamic gonadotropin releasing hormone and corticotropin releasing hormone. It causes increase of somatotropin secretion, luteinizing hormone and foliculotropin release and adrenocorticotropin secretion. The hypothalamic galanin takes part in etiopathogenesis of obesity not only in human reproductive period, but also in adolescence, increasing the appetite and changing fat metabolism. This variety of actions emphasizes the potential importance of this peptide in the regulation of cells function and the need to understand the mechanism by which they act.
Endokrynol Diabetol Chor Przemiany Materii Wieku Rozw 2000
PMID:[The role of galanin in the endocrine system]. 1281 74

The authors describe the case of a 14-year old girl with pseudohypoparathyroidism, who showed characteristic phenotypic features of Albright's hereditary osteodystrophy (short stature, round face, mild obesity, abnormal position of teeth, lack of canines, limb valgity) and biochemical disturbances--hypocalcemia, hyperphosphatemia. The nature of pseudohypoparathyroidism consists in a lack of response to the parathormone of effector organs, such as kidneys, bones, alimentary tract. The treatment of choice includes active metabolites of vitamin D3, calcium salts, phosphate-binding components. Pseudohypoparathyroidism is a rare disease. Worth noting is the fact that it can occur in a child with height deficiency.
Endokrynol Diabetol Chor Przemiany Materii Wieku Rozw 1999
PMID:[Pseudohypoparathyroidism in a 14-year old girl]. 1281 2

The aim of the study was to estimate growth curve and body mass during and after a treatment of ALL. Retrospective study group included 48 children (27 boys and 21 girls). The age at the start of the treatment varied from 1.4 up 17 years, during our evaluation 4.6-25.4 years. Patients were treated according to modified American (New York Protocol) and German (BFM) protocols. 43 children received central nervous system radiation in a dose of 14-24 Gy. All children completed the treatment protocol and are in the remission. Growth velocity and body mass were estimated during and after the ALL treatment. During the treatment growth retardation was observed at 34 children (2/3 patients). No significant difference in growth velocity was found between group of standard and high risk of ALL. Combined radiotherapy and chemotherapy has probably more influence for growth retardation than chemotherapy alone. Obesity was stated at 13 patients (27%), mostly boys. After the treatment 9 children were permanently obese. Body mass deficiency was found at 5 patients during the treatment and was the same when the treatment protocol was completed.
Endokrynol Diabetol Chor Przemiany Materii Wieku Rozw 2001
PMID:[Evaluation of growth and body weight in children and adolescent during and after treatment of acute lymphoblastic leukemia]. 1281 37

Adolescents with type 1 diabetes mellitus, especially diabetic pubertal girls, have been found to be more prone to high body mass index than their non-diabetic peers. It is an important problem because it has been associated with risk of cardiovascular complications and other. The study was performed in 93 diabetic girls aged from 14 to 18 years, duration of diabetes varied from 6.4 to 7.7 years. The control group consisted of 75 non diabetic girls matched for age. Girls with type 1 diabetes are more overweight than their peers. In the non diabetic subjects BMI was 20.60+/-0.24 kg/m2, in the diabetic girls BMI was significantly higher, mean 22.70+/-0.23 kg/m2, which indicates a need of more effective prevention of obesity in diabetic children and adolescents, especially in pubertal girls.
Endokrynol Diabetol Chor Przemiany Materii Wieku Rozw 2001
PMID:[Overweight - problem in pediatric patients. Part II. Weight gain in insulin treatment of adolescent diabetic girls]. 1281 51

The metabolic syndrome is a highly prevalent clinical entity. The recent Adult Treatment Panel (ATP III) guidelines have called specific attention to the importance of targeting the cardiovascular risk factors of the metabolic syndrome as a method of risk reduction therapy. The main factors characteristic of this syndrome are abdominal obesity, atherogenic dyslipidemia, elevated blood pressure, insulin resistance (with or without glucose intolerance), prothrombotic and proinflammatory states. An insulin resistance following nuclear peroxisome proliferator activated receptors (PPAR) deactivation (mainly obesity-related) is the key phase of metabolic syndrome initiation. Afterwards, there are 2 principal pathways of metabolic syndrome development: 1) with preserved pancreatic beta cells function and insulin hypersecretion which can compensate for insulin resistance. This pathway leads mainly to the macrovascular complications of metabolic syndrome; 2) with massive damage of pancreatic beta cells leading to progressively decrease of insulin secretion and to hyperglycemia (e.g. overt type 2 diabetes). This pathway leads to both microvascular and macrovascular complications. We suggest that a PPAR-based appraisal of metabolic syndrome and type 2 diabetes may improve our understanding of these diseases and set a basis for a comprehensive approach in their treatment.
Cardiovasc Diabetol 2003 Mar 23
PMID:Metabolic syndrome and type 2 diabetes mellitus: focus on peroxisome proliferator activated receptors (PPAR). 1283 41


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>