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

Obese subjects were compared with lean subjects to define the previously reported disturbance of plasma free fatty acid (FFA) kinetics in terms of altered net transport (lipolysis) or clearance (esterification). These measurements were made during prolonged constant infusions of 1--14C-palmitate toward the end of sustained glucose ingestion and again 6-8 hr after stopping glucose. Net transport of FFA was suppressed to equally low levels in obese and lean subjects, though at the expense of higher insulin concentrations in the obese. Whereas in the lean subjects the clearance of FFA was significantly stimulated with glucose, the obese subjects showed low clearance rates both during and after stopping glucose. When glucose was stopped, net transport rose more rapidly and to a greater extent in some obese than in the lean subjects. The increased influx of FFA led to a rise in the plasma triglyceride level only in the lean subjects. These studies suggest that clearance of plasma FFA, probably denoting esterification in tissues such as muscle and adipose tissue, is impaired in obesity and cannot be readily stimulated with glucose and insulin. Lipolysis, measured as net transport of FFA, however, is suppressible with glucose and insulin in the obese, though this might be achieved only at insulin levels that are higher than those in lean subjects.
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PMID:Diminished plasma free fatty acid clearance in obese subjects. 64 29

Reduced thermogenesis in brown adipose tissue (BAT) may contribute to increased energetic efficiency and obesity in rats with ventromedial hypothalamic (VMH) lesions. Thermogenic activity of BAT is a function of the environmental temperature. If a relationship exists, it follows that the increased energetic efficiency of VMH-lesioned rats likewise should be governed by temperature. We have therefore investigated the energy balance of normal and VMH-lesioned rats housed at 30 degrees C and 10 degrees C. Experiments at differing feeding levels allowed calculation of maintenance energy requirements and the net energetic efficiencies of each group. VMH-lesioned rats at thermoneutrality (30 degrees C) accumulated more body fat at all feeding levels than did normal rats. Maintenance energy requirement was reduced, but the net energetic efficiency did not differ significantly from normal. The reduced maintenance energy requirement of lesioned rats persisted at 10 degrees C. Net energetic efficiency decreased in normal rats acclimated to cold but increased in the lesioned group. The difference was significant (P less than 0.05). The cold-induced increase in interscapular brown adipose tissue (IBAT) oxidative capacity of VMH-lesioned rats was only half that of normal rats. Differences in BAT thermogenesis may be the basis for the differing temperature effects on net energetic efficiency.
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PMID:Opposite effect of cold on energetic efficiency in normal and obese Wistar rats with hypothalamic lesions. 200 9

Studies were conducted to determine whether metabolic adaptation occurred in the hypothalamus of overfed parabiotic rats and their partners to distinguish between the adaptations caused by increased caloric intake and those caused by the production of a "lipostatic factor." The induction of overfed obesity in one parabiotic partner was employed to test the hypothesis that a putative lipostatic factor produced in the obese parabiotic elicited the hypophagic-lipid-mobilizing effect observed in the lean parabiotic via alterations in hypothalamic fatty acid and glucose metabolism. Fatty acid oxidation in the ventrolateral hypothalamus (VLH) of overfed parabiotic rats and their partners was lower than in ad libitum parabiotic rats. Net flux of glucose through the VLH gamma-aminobutyric acid (GABA) shunt was elevated in overfed parabiotic rats compared with the net flux observed in their partners and ad libitum parabiotic rats, the levels being similar in these last two groups. Net flux of glucose through the ventromedial hypothalamic (VMH) pentose shunt in overfed parabiotic rats and their partners was elevated relative to ad libitum parabiotic rats. The putative lipostatic factor may act to regulate energy balance through modification of VLH fatty acid oxidation and/or glucose flux via the VMH pentose shunt.
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PMID:Site of action of putative lipostatic factor: hypothalamic metabolism of parabiotic rats. 254 57

Female pigs were selected at birth from litters of genetically lean and obese and contemporary commercial-type pigs to quantify the biweekly changes in fasting concentrations of plasma glucose, immunoreactive insulin, triglyceride and cholesterol during the growing period (birth to 22 weeks of age). Pigs were weaned at 4 weeks of age to a standard corn-soybean meal type dry diet fed ad libitum. Four pigs from each genetic group were used at weeks 4 and 16 of age for a standard oral glucose tolerance test. Plasma concentrations of glucose, insulin, triglyceride and cholesterol were generally similar in all breed from birth to 22 weeks of age. Overall means (N = 306) were: glucose 93.2 mg/dl; triglyceride 37.5 mg/dL, cholesterol 101.8 mg/dL and insulin 10.8 micron Units/ml. There were significant breed differences in a given plasma variable at individual sampling periods, but most were not sustained at earlier or later ages. The genetically lean pigs had lower insulin and triglyceride levels, especially at older ages. Glucose clearance from the plasma at 4 and 16 weeks of age was similar in the three breed groups. It is concluded that these genetically obese pigs selected for fatness over many generations do not manifest their propensity to obesity through modifications in circulating glucose, insulin, triglyceride or cholesterol. Net differences in body fat accretion between these genetically lean and obese populations apparently reside in adipocyte metabolism and are not complicated by an inability to maintain homeostasis of plasma glucose or lipids as is the case with many animal models for obesity. This population of obese and lean swine selected for many generations from a common parental population appears to be a useful model for studies of the metabolic bases of obesity.
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PMID:Plasma glucose, insulin and lipids during growth of genetically lean and obese swine. 675 63

Ad libitum access to a high-fat (HF) diet produces a wide range of weight gain in rats. Rats most susceptible to weight gain on such a diet (obesity prone; OP) are more insulin resistant after 4-5 wk of diet exposure than are those most resistant (obesity resistant; OR) to weight gain. To investigate whether skeletal muscle glucose metabolism contributes to insulin resistance in this model, insulin-stimulated glucose metabolism was assessed in the perfused hindquarter of rats exposed to either a low-fat (LF, n = 6) or HF diet for 5 wk. Delineation of OP (n = 6) and OR (n = 6) rats was based on body weight gain. OP rats gained 60% more body weight while eating only 10% more energy than OR rats. Single-pass perfusions were carried out for 2 h in the presence of glucose, insulin, and [U-14C]glucose. Insulin-stimulated glucose uptake (mumol.100 g-1.min-1) was 14.2 +/- 0.9 in LF, 11.1 +/- 0.8 in OR, and 6.2 +/- 0.6 in OP. Glucose oxidation (mumol.100 g-1.min-1) was 1.7 +/- 0.3 and 1.2 +/- 0.3 in LF and OR, respectively, but was 0.2 +/- 0.1 in OP. Net glycogen synthesis was significantly reduced in OP compared with OR and LF despite similar glycogen synthase I activity. Muscle triglyceride concentration was not significantly different in OR and OP rats. These results demonstrate significant defects in skeletal muscle glucose uptake and disposal in rats most susceptible to HF diet-induced obesity. Clearly, the heterogeneous response to a HF diet involves not only body weight gain but also skeletal muscle fuel metabolism.
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PMID:Skeletal muscle glucose metabolism in obesity-prone and obesity-resistant rats. 832 78

Most of the available appetite-suppressant drugs act on noradrenergic and possibly dopaminergic receptors to produce satiety. A smaller number increase excess neuronal serotonin levels by blocking serotonin reuptake or by increasing its release. All these drugs produce significantly greater weight loss than does placebo in most studies. Abuse is a problem with amphetamine, methamphetamine, and benzphetamine, whereas other drugs have minimal or no potential for abuse. Weight loss can be sustained for up to 36 months. Net weight loss, compared with placebo, ranges from 2 to 10 kg, and weight regain after terminating drug treatment proves that drugs do not work when not taken. The stigma of obesity, the public opprobrium toward obese persons, and regulatory rigidity have led to unjustified distrust in the potential of drug treatment for obesity.
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PMID:Use and abuse of appetite-suppressant drugs in the treatment of obesity. 836 2

Based on previous cross-sectional findings, we hypothesized that weight loss could improve several hemostatic factors associated with cardiovascular disease. In a randomized controlled trial, moderately overweight men and women were assigned to one of four weight loss treatment groups or to a control group. Measurements of plasminogen activator inhibitor-1 (PAI-1) antigen, tissue-type plasminogen activator (t-PA) antigen, D-dimer antigen, factor VII activity, fibrinogen, and protein C antigens were made at baseline and after 6 months in 90 men and 88 women. Net treatment weight loss was 9.4 kg in men and 7.4 kg in women. There was no net change (p > 0.05) in D-dimer, fibrinogen, or protein C with weight loss. Significant (p < 0.05) decreases were observed in the combined treatment groups compared with the control group for mean PAI-1 (31% decline), t-PA antigen (24% decline), and factor VII (11% decline). Decreases in these hemostatic variables were correlated with the amount of weight lost and the degree that plasma triglycerides declined; these correlations were stronger in men than women. These findings suggest that weight loss can improve abnormalities in hemostatic factors associated with obesity.
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PMID:Impact of weight loss on plasminogen activator inhibitor (PAI-1), factor VII, and other hemostatic factors in moderately overweight adults. 842 53

Impaired stimulation of glucose metabolism and reduced suppression of lipolytic activity have both been suggested as important defects related to the insulin resistance of adolescent obesity. To further explore the relationship between these abnormalities, we studied seven obese [body mass index (BMI) 35 +/- 2 kg/m2] and seven lean (BMI 21 +/- 1 kg/m2) adolescents aged 13-15 yr and compared them with nine lean adults (aged 21-27 yr, BMI 23 +/- 1 kg/m2) during a two-step euglycemic-hyperinsulinemic clamp in combination with 1) a constant [2H5]glycerol (1.2 mg.m-2.min-1) infusion to quantify glycerol turnover and 2) indirect calorimetry to estimate glucose and net lipid oxidation rates. In absolute terms, basal glycerol turnover was increased and suppression by insulin was impaired in obese adolescents compared with both groups of lean subjects (P < 0.01). However, when the rates of glycerol turnover were adjusted for differences in body fat mass, the rates were similar in all three groups. Basal plasma free fatty acid (FFA) concentrations were significantly elevated, and the suppression by physiological increments in plasma insulin was impaired in obese adolescents compared with lean adults (P < 0.05). In parallel with the high circulating FFA levels, net lipid oxidation in the basal state and during the clamp was also elevated in the obese group compared with lean adults. Net lipid oxidation was inversely correlated with glucose oxidation (r = -0.50, P < 0.01). In conclusion, these data suggest that lipolysis is increased in obese adolescents (vs. lean adolescents and adults) as a consequence of an enlarged adipose mass rather than altered sensitivity of adipocytes to the suppressing action of insulin.
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PMID:Effect of insulin on glycerol production in obese adolescents. 957 36

Energy supply from foods and drinks depends upon carbohydrate, protein, lipid and alcohol content. Cells obtain the energy through a complex and integrated system of physico-chemical processes. The energy value of foods is applied for ATP formation, but also for nutrient utilization and turnover. Net energy from foods is expended for basal metabolism, thermic effect of food and physical activity. Total energy expenditure for human beings is displayed in different lists developed by national and international organisms and institutions. Energy balance and body weight are narrowly interrelated as well as body composition, which depends also of age, sex, exercise and neuroendocrine status. Obesity, is known as an excessive deposition of fat for height, and it is associated with cancer, dislipemias, endocrine abnormalities, diabetes, etc. Recent advances suggest that genetic and neuroendocrine factors are more involved in obesity rather than gluttony or sloth as previously reported.
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PMID:[Nutrition, energy balance, and obesity]. 1042 Sep 25

Humans can maintain health on diets differing widely in their macronutrient content, and numerous diet recommendations have been made to maintain health and to help weight control. Net adenosine triphosphate yields during the oxidation of carbohydrate, fat, and protein come to 75%, 90%, and 55%, respectively. However, macronutrient proportions can only be varied within limits, and differences in energy dissipation achievable by macronutrient exchanges are minor. In the National Health and Nutrition Examination Survey III data, stature explains 10% to 16% of the variance in fat-free mass in adults (the most significant predictor of resting energy expenditure), but <1% of the variance in the percentage of body fat. Thus, differences in resting energy expenditure cannot be expected to have much effect on adiposity. Recommendations designed to facilitate weight control, therefore, should be based on their potential impact on food consumption and energy intake. They should also reflect the fact that the logic for nutrient selection is not the same during weight maintenance and weight reduction. Glycogen levels, along with inherited traits and exercise habits, influence fat oxidation, and, hence, the size that the adipose tissue mass has to reach for fat oxidation to become commensurate with fat intake. Recent increases in the prevalence of obesity could have been brought about by the effect of changes in the food supply and by further declines in physical activity on habitual glycogen levels. Given that biological evolution led to food intake regulating mechanisms that are more powerful in promoting search for food than in seeking to restrain energy intake, it is not surprising that constant availability of desirable foods would lead to a high prevalence of obesity.
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PMID:Macronutrient composition and food selection. 1170 51


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