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Query: UMLS:C0028754 (
obesity
)
124,988
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
A number of biochemical defects have been identified in glucose metabolism within skeletal muscle in
obesity
, and positive effects of weight loss on insulin resistance are also well established. Less is known about the capacity of skeletal muscle for the metabolism of fatty acids in
obesity
-related insulin resistance and of the effects of weight loss, though it is evident that muscle contains increased triglyceride. The current study was therefore undertaken to profile markers of human skeletal muscle for fatty acid metabolism in relation to
obesity
, in relation to the phenotype of insulin-resistant glucose metabolism, and to examine the effects of weight loss. Fifty-five men and women, lean and obese, with normal glucose tolerance underwent percutaneous biopsy of vastus lateralis skeletal muscle for determination of HADH, CPT, heparin-releasable (Hr) and tissue-extractable (Ext) LPL, CS, COX, PFK, and GAPDH enzyme activities, and content of cytosolic and plasma membrane FABP. Insulin sensitivity was measured using the euglycemic clamp method. DEXA was used to measure FM and
FFM
. In skeletal muscle of obese individuals, CPT, CS, and COX activities were lower while, conversely, they had a higher or similar content of FABP(C) and FABP(PM) than in lean individuals. Hr and Ext LPL activities were similar in both groups. In multivariate and simple regression analyses, there were significant correlations between insulin resistance and several markers of FA metabolism, notably, CPT and FABP(PM). These data suggest that in
obesity
-related insulin resistance, the metabolic capacity of skeletal muscle appears to be organized toward fat esterification rather than oxidation and that dietary-induced weight loss does not correct this disposition.
...
PMID:Markers of capacity to utilize fatty acids in human skeletal muscle: relation to insulin resistance and obesity and effects of weight loss. 1054 88
A comparative investigation of 99 normotensive and 111 hypertensive Bengalee Hindu elderly men (aged 55 years and above) of Kalighat, South Calcutta, India, was undertaken to study differences in levels of adiposity, body fat distribution and body composition between these two groups. Results revealed that there were significant differences between normotensive (NT) and hypertensive (HT) subjects in the mean values for weight (p < 0.05), body mass index (BMI, p < 0.01); waist (p < 0.001) and hip circumferences (p < 0.05); waist-hip ratio (WHR, p < 0.001), conicity index (CI, p < 0.01) and fat free mass (
FFM
, p < 0.001). Percentile distributions for all these variables and indices showed consistently higher values among the HT patients as compared with NT subjects. However, the frequency of
obesity
(BMI > or = 25) was similar (NT = 6.1%, HT = 11.7%) in both groups. Thus, these results indicated that there existed significant differences in central adiposity and
FFM
between NT and HT subjects although their level of
obesity
was similar. Hypertensive individuals have significantly enhanced levels of central body fat distribution.
...
PMID:Comparison of anthropometric characteristics between normotensive and hypertensive individuals among a population of Bengalee Hindu elderly men in Calcutta, India. 1094 84
Recent findings have questioned the independent influence of insulin on leptin. We studied whether insulin contributes to leptin in obese children, independent of confounding parameters, such as total adiposity, fasting insulin resistance index, and fat free mass. In 100 obese boys and 103 obese girls, blood levels of leptin, insulin, glucose, and triglycerides were determined. The fasting insulin resistance index (FIRI) was calculated, and body composition was assessed by means of impedance. Leptin and glucose were higher in girls, and all estimates of adiposity were significantly associated with leptin. However, when adjusted for adiposity, the relationship between insulin and leptin, and also between FIRI and leptin, remained significant in boys and girls (p<0.05). Although several regression models were tested, neither insulin nor FIRI were found to contribute significantly and independently to leptin. BMI together with triglycerides and
FFM
were the main determinants for the variation in leptin in boys (adj. R2=0.46, p<0.0001). In girls, BMI explained a great magnitude of the variation in leptin (adj. R2=0.60, p<0.0001). These findings indicate that in the state of childhood and adolescent
obesity
, total adiposity but not insulin or insulin resistance index is the main determinant for leptin. In contrast to obese girls, the fat free mass and triglycerides contribute significantly to the variation in leptin in obese boys. The biological significance for these findings should be elucidated in longitudinal studies.
...
PMID:Insulin and insulin resistance index are not independent determinants for the variation in leptin in obese children and adolescents. 1096 81
Regular physical activity has profound effects on body composition and the utilisation of nutrients and help to maintain and increase skeletal muscle mass, with increased resting metabolic rate and enhanced capacity for lipid oxidation during rest and exercise. Regular exercise may also prevent or limit the loss of lean tissue (fat-free mass,
FFM
) during slimming regimens. Increased physical activity induces a number of favourable changes in the metabolism of lipoproteins: serum triglycerides are lowered by the increased lipolytic activity, the HDL concentration increases and the concentration of small dense LDL decreases. In addition, the enhanced metabolic capacity of skeletal muscle (metabolic fitness) will favorably influence risk factors such as insulin resistance and hypertension. Because regular physical activity has favorable effects on several of the comorbid conditions of
obesity
, particularly cardiovascular disease and type 2 diabetes, it is not surprising that the mortality rates seem to be lower in the overweight and moderately obese individuals who are physically fit compared with the unfit. The treatment of overweight and obese persons should perhaps be more focused on the level of regular physical activity than on body weight per se. For most of those who wish to reduce their body weight, it is recommended that they combine regular physical activity with a somewhat reduced energy intake, in particular of food rich in fat. Emphasis should be on promoting relatively low-intensity, long-duration physical activity which can be conveniently incorporated into daily life.
...
PMID:[Physical activity, overweight and obesity]. 1118 89
The purpose of this study was to examine the rates of substrate oxidation in lean and obese women during short-duration, high-intensity exercise and to examine the effects of a 16-week exercise training program on substrate oxidation during 30 min of exercise in lean and obese individuals. Fat and carbohydrate oxidation were measured in 8 non-obese (Non-Ob), 11 lower-body obese (LBO) and 12 upper-body obese (UBO) women at rest and during 30 min of treadmill exercise at 70% of peak oxygen uptake. The obese women participated in 16 weeks of aerobic training (3 times per week at 70% of maximum oxygen uptake). Total fat and carbohydrate oxidation were measured using indirect calorimetry. The respiratory exchange ratio (R) was similar between groups at rest and was found to decrease throughout the exercise session (P< 0.01). Fat oxidation was greater at 15 min of exercise than at rest (P<0.01) but did not increase significantly more at 30 min of exercise.
Obese
women had significantly greater fat oxidation (both absolute concentrations and when expressed per kg of fat free mass,
FFM
) at 30 min of exercise than the Non-Ob women [Non-Ob 23.5 (3.7) micromol.kg
FFM
(-1).min(-1), LBO 35.2 (3.1) micromol.kg
FFM
(-1).min(-1), UBO 33.2 (2.6) micromol.kg
FFM
(-1).min(-1); P<0.01]. Carbohydrate oxidation also increased (P < 0.01) in response to exercise, but no group differences were found. The pattern of fat distribution (LBO vs UBO) did not affect the resting or exercise fat oxidation (P=NS). Sixteen weeks of aerobic exercise did not result in significant changes in resting or exercise fat oxidation in the obese women (n = 10; P=NS), but did significantly increase carbohydrate oxidation [pretraining 8.6 (1.4) micromol.kg
FFM
(-1), post-training 13.6 (2.1) micromol.kg
FFM
(-1).min(-1); P<0.01]. Unlike earlier studies, this shorter-duration, higher-intensity exercise resulted in a greater whole-body fat oxidation in the obese women than in the Non-Ob women, and exercise training did not result in any changes in fat oxidation, but did increase exercise carbohydrate oxidation.
...
PMID:Substrate oxidation during acute exercise and with exercise training in lean and obese women. 1151 23
In obese humans, insulin resistance is accompanied by elevated levels of plasma cell membrane glycoprotein (PC-1) and decreased insulin receptor (IR) tyrosine kinase activity in skeletal muscle. PC-1 overexpression inhibits IR tyrosine kinase and possibly other downstream signaling events. The rhesus monkey in captivity is susceptible to
obesity
with concomitant insulin resistance. In the present study we analyzed obese (n = 10, 29.4% +/- 1.2% body fat) and non-obese (n = 12, 19.4% +/- 1.9% body fat) rhesus monkeys. Glucose clearance during an euglycemic hyperinsulinemic (400 mU/m(2) body surface area/min) clamp was lower for the obese group (non-obese, 9.7 +/- 0.9; obese, 3.2 +/- 0.7 mg/kg fat-free mass [
FFM
]/min; P <.01). We performed vastus lateralis muscle biopsies prior to and during the clamp. We measured PC-1 levels in these muscle samples to determine whether PC-1 content is elevated in this primate model of insulin resistance. PC-1 levels were determined by assay of phosphodiesterase activity and specific PC-1 enzyme-linked immunosorbent assay (ELISA). In the obese group, both PC-1 content and activity were 2-fold higher than in the non-obese group (P <.05). In order to investigate the ability of insulin to stimulate IR signaling in vivo in these 2 groups of monkeys, we then measured tyrosine autophosphorylation of the IR by specific ELISA. The increase in IR autophosphorylation in the non-obese group was twice that of the obese group (fold increase over basal: non-obese, 3.7 +/- 0.3; obese, 1.9 +/- 0.6; P <.05). We conclude that insulin resistance secondary to
obesity
in rhesus monkeys is associated with increased levels of PC-1 and decreased IR signaling capacity in skeletal muscle.
...
PMID:Elevated plasma cell membrane glycoprotein levels and diminished insulin receptor autophosphorylation in obese, insulin-resistant rhesus monkeys. 1191 55
We have previously shown that sex and
obesity
independently affect basal very low density lipoprotein (VLDL)-triglyceride (TG) kinetics. In the present study, we investigated the effect of hyperglycemia-hyperinsulinemia on VLDL-TG kinetics in lean and obese men and women (n = 6 in each group). VLDL-TG kinetics were measured during basal, postabsorptive conditions and during glucose infusion (5.5 mg x kg
FFM
(-1) x min(-1)) by using [(2)H(5)]glycerol bolus injection in conjunction with compartmental modeling analysis. Basal VLDL-TG secretion in plasma was greater in obese than in lean men (7.8 +/- 0.6 and 2.9 +/- 0.4 micromol x l plasma(-1) x min(-1); P < 0.001) but was not different in lean and obese women (5.0 +/- 1.1 and 5.9 +/- 1.1 micromol x l plasma(-1) x min(-1)). Glucose infusion decreased the VLDL-TG secretion rate by approximately 50% in lean and obese men and in lean women (to 1.5 +/- 0.4, 4.0 +/- 0.6, and 2.2 +/- 0.4 micromol x l plasma(-1) x min(-1), respectively; all P < 0.05) but had no effect on the VLDL-TG secretion rate in obese women (4.9 +/- 1.0 micromol x l plasma(-1) x min(-1)). These results demonstrate that both sex and adiposity affect the regulation of VLDL-TG metabolism. Glucose and insulin decrease VLDL-TG production in both lean men and lean women;
obesity
is associated with resistance to the glucose- and insulin-mediated suppression of VLDL-TG secretion in women, but not in men.
...
PMID:VLDL-triglyceride kinetics during hyperglycemia-hyperinsulinemia: effects of sex and obesity. 1247 56
Insulin resistance is a key element of metabolic syndrome, which includes disturbances of glucose tolerance,
obesity
, hypertension, coronary heart disease dyslipidemia and many other defects. An important problem in scientific research is precise measurement of insulin sensitivity. The method considered "the gold standard" is glucose clamp, however, it is difficult to apply this method in large studies. Therefore, simple indices of insulin resistance are proposed. It remains unclear whether those indices are able to reflect changes occurring during insulin-sensitizing intervention. The aim of the present study was to assess the use of indirect indices for the changes in insulin sensitivity during exercise training and to compare those indices with results derived from clamp. Fourteen obese normoglycemic women participated in 12-week exercise training program, which included exercise performed on a bicycle ergometer, 5 days a week for 30 minutes. Insulin sensitivity (M/
FFM
value) before and after training was measured with hyperinsulinemic euglycemic clamp technique. Simple indices of insulin resistance were also assessed: fasting plasma insulin (INS), logarithm INS (log [INS]), homeostasis model assessment (HOMA), logarithm HOMA (log [HOMA]) and quantitative insulin sensitivity check index (QUICKI). Before training, all those indices were markedly related to M/
FFM
. After training, an increase in M/
FFM
was observed. None of the examined indices markedly changed after training. There was no correlations between changes of evaluated indices and in M/
FFM
during training, and no relationships of those parameters after training. Our study indicates that simple indices are not able to reflect changes occurring during insulin-sensitizing intervention.
...
PMID:[Assessment of insulin sensitivity during exercise training program in obese women. Comparison of simple indices with hyperinsulinemic euglycemic clamp technique]. 1476 77
Non syndromic forms of Retinitis Pigmentosa (RP) constitute a collection of clinically and genetically heterogeneous inherited retinal degenerative diseases. They are characterized by a bilateral progressive visual loss susceptible to cause blindness. These diseases are transmitted through pedigrees according to all known modes of inheritance. They are bilateral and usually start during infancy. However, very early clinical presentations exist, such as those observed in children affected by Leber Congenital Amaurosis, as well as late onset autosomal dominant forms of retinitis pigmentosa. The characteristic clinical aspect of the rod-cone RP dystrophies is marked by alterations of the peripheral retina associated with a night blindness and a progressive narrowing of the visual field. The ophthalmoscopic examination of RP patients commonly reveals thin retinal arteries and scattered pigmentary accumulations. In contrast, there are cone rod retinal dystrophies whose onset is marked by a decreased visual acuity before the appearance of any visual field alteration. Some forms of RPs display an ocular fundus devoid of any pigmentary alteration. Syndromic forms of RPs are not uncommon. The association of deafness with RP is detected in nearly 30% of the patients. Other associations with RP can include mental deficiency, facial dysmorphy, microcephaly,
obesity
, kidney deficiency, immune deficiencies, metabolic disorders. The existence of such syndromic forms of RP localizes RPs at the crossroad of several medical specialties. A long lasting collaboration between our department of ophthalmology and the department of medical genetics of the Necker-Sick Children Hospital has allowed us to establish numerous genotype-phenotype correlations, especially in LCA and Stargardt's disease.
ABCR
gene mutations cause Stargardt disease.
ABCR
mutations may also cause some types of Ages Related Macular Degenerations (AMD). Nowadays, there is no known efficient therapy available for patients affected by RP. Gene therapies hold promises of treatment for patients affected by some of these diseases for the next decade. In a not too far future, the use of pharmacological drugs increasing a better intracellular oxygen availability, without triggering any harmful production of free radical oxygen species (ROS), while exerting an anti-apoptotic effect within photoreceptor cells, appears to be a therapeutical strategy deserving to be tested in an appropriately designed clinical trial. For the present time, optical and electronical devices as well as night-vision glasses are the only possible tools allowing to improve the quality of life of some patients.
...
PMID:[Early therapeutic trials for retinitis pigmentosa]. 1536 38
Magnetic resonance imaging (MRI) can be used to assess metabolically active components of
FFM
. MRI-derived organ mass (OM) explains part of the interindividual variance in REE. It may also add to our understanding of malnutrition- and
obesity
-related variance in REE. There is need for (i) standardisation of MRI technology in body composition research, (ii) reference data on detailed body composition including also more recent autopsy data, (iii) reducing the number of assumptions in model-based predictions and (iv) a combination of imaging technologies with in vivo measurements of individual OM respiration (e.g. by positron emission tomography).
...
PMID:Metabolically active components of fat free mass (FFM) and resting energy expenditure (REE) in humans. 1580 10
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