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

Thermogenesis (adaptive increases in heat production) can develop in response to low environmental temperature, alterations in the amount or composition of the diet, and pathogenic stimuli, such as infection, injury, and inflammation. Thermogenic responses to each of these stimuli appear to be mediated by activation of the sympathetic nervous system and, at least in experimental animals, by heat production in brown fat. Thermogenesis is under the direct control by the central nervous system (CNS), particularly by specific regions of the hypothalamus. Serotonergic pathways have been directly implicated in the central control of most forms of thermogenesis, and indirect evidence suggests involvement of adrenergic and cholinergic mechanisms. Numerous peptides have been shown to induce increases on metabolic rate when injected into the brains of experimental animals; of these, corticotrophin-releasing factor (CRF) has been the most extensively studied. CRF appears to mediate thermogenic responses to serotonergic agonists, injury, and cytokines, and may be involved in impaired thermogenic responses in certain genetically obese rodents. Cytokines, particularly interleukin-1 (IL-1) and IL-6, act as endogenous pyrogens in the brain and stimulate thermogenesis via synthesis of prostaglandins and CRF. Peptides such as lipocortin-1, arginine vasopressin, and alpha MSH potently inhibit central effects of cytokines. Pharmacological modification of thermogenesis may be clinically beneficial in treating conditions such as obesity, cachexia, and fever.
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PMID:CNS regulation of thermogenesis. 812 29

A descriptive term nonbacterial thrombotic endocarditis (NBTE) is used currently instead of the former name marantic endocarditis. The study describes 171 cases of NBTE encountered in autopsies over a period of 22 years (an incidence of 0.93% in adults). Malignancy was present in 59% of cases. Tumors relatively most frequently associated with NBTE were carcinomas of the ovaries, biliary system, pancreas, lung, and stomach. The vegetations were located mostly on the left-sided valves (mitral 64%, aortic 24%, both 9%). The involved valves were otherwise normal in 82%, and they were previously damaged in 18%. Systemic emboli from valvular vegetations occurred in 41% of patients, with splenic, cerebral, and renal circulations being most frequently affected. Pulmonary embolism was noted in 43%. The state of nutrition at autopsy was within normal limits in 35%; there was undernourishment or cachexia in 40%, and overweight or obesity in 22% of patients. The main pathogenetic factor in NBTE seems to be a state of hypercoagulation.
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PMID:[Nonbacterial thrombotic endocarditis--a study of 171 case reports]. 833 26

Some conditions that predispose to ventilatory failure increase the work of breathing (chronic obstructive pulmonary disease [COPD], obesity, kyphoscoliosis), whereas others cause severe respiratory muscle weakness. Specific reasons for muscle weakness include critical illness (electrolyte imbalance, acidemia, shock, sepsis), chronic illness (poor nutrition, cachexia), and neuromuscular diseases. Inspiratory muscle weakness from mechanical disadvantage to the diaphragm is characteristic of asthma and COPD. The increased work of breathing combined with muscle weakness increases the pressure needed to inspire a breath and decreases maximal inspiratory pressure. When this pressure exceeds 0.4, dyspnea and inspiratory muscle fatigue ensue. One way to lower this pressure and avert fatigue is to lower the tidal volume. Ventilatory drive is high, not low, in ventilatory failure. Concomitant shortening of inspiration and breath duration cause the small tidal volume and increased respiratory rate. Gas exchange is compromised by ventilation/perfusion imbalance, and the ratio of dead space to tidal volume is also increased by rapid, shallow breathing. Reduction in tidal volume minimizes dyspnea, but the small tidal volume is inadequate for gas exchange. Acute treatment of respiratory muscle failure involves respiratory muscle rest through mechanical ventilation and removal of noxious influences (infection, metabolic disarray), whereas chronic treatment involves rebuilding the contractile apparatus by nutritional repletion and training.
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PMID:Respiratory muscles and ventilatory failure: 1993 perspective. 850 1

Cachexia is a common cause of morbidity and mortality in cancer patients. Successful nutritional repletion might enhance treatment results, quality of life, and survival. In the past, attempts at nonvolitional feeding (enteral and parenteral techniques) have not been as successful as initially hoped. The cachectic cancer patient's loss of lean body mass has been very difficult to restore, although fat can be repleted. Laboratory and epidemiologic investigations have suggested that dietary calories and dietary fat may play a promotional role in cancer. Overfed animals and obese humans both have an increased tendency for development of malignancy. Breast cancer has been investigated extensively for its relationship to diet. Certain fatty acids appear to stimulate breast cancer, as do obesity-related changes in circulating hormones. Obesity in breast cancer and weight gain on adjuvant therapy may therefore be adverse prognostic signs. Clinical trials of decreasing dietary fat as an adjuvant to breast cancer therapy are in progress. The current challenge in nutritional management of the cancer patient is to incorporate laboratory, epidemiologic, and clinical data into a successful repletion strategy. It seems unlikely that traditional methods of supplying excess calories will succeed, so that other, more specific nutritional manipulations should be evaluated in clinical trials.
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PMID:Cancer, cancer cachexia, and diet: lessons from clinical research. 885 Feb 22

Neuropeptide Y (NPY) neurones in the arcuate nucleus of the rodent hypothalamus may play a key role in responding to reductions in body energy stores with appropriate changes in energy homeostasis, namely an increase in food-seeking behaviour and hyperphagia, together with a reduction in heat production by brown adipose tissue. These adaptive responses are mimicked by the injection of NPY into the main sites of projection of the NPY neurones, and animals that are threatened by energy deficits (e.g. through starvation or insulin-deficient diabetes) show increased activity of these neurones. Genetically obese rodents also show hyperactivity of the NPY neurones, which is inappropriate to their energy needs and may contribute to their hyperphagia, reduced energy expenditure and excessive weight gain. The NPY neurones may be inhibited by insulin and leptin, which may both serve as signals of peripheral fat mass. Ultimately, characterization of the specific "feeding' receptors which mediate NPY's central effects on energy homeostasis may provide opportunities for designing drugs to manipulate and appetite and energy balance in man, notably obesity and the cachexia commonly associated with malignancy and chronic infection.
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PMID:Neuropeptide Y, the hypothalamus and the regulation of energy homeostasis. 887 Nov 82

An increase in the sensation of hunger and overeating after a period of chronic energy deprivation can be part of an autoregulatory phenomenon attempting to restore body weight. To gain insights into the role of fat and lean tissue depletion as determinants of such a hyperphagic response in humans, we reanalyzed the individual data on food intake and body composition available for the 12 starved and refed men in the classical Minnesota Experiment after a shift from a 12-wk period of restricted refeeding to an ad libitum refeeding period of 8 wk. For each individual, the following were determined: 1) the total hyperphagic response during the ad libitum refeeding period, calculated as the energy intake in excess of that during the prestarvation (control) period; 2) the degree of fat recovery and that of fat-free-mass (FFM) recovery before ad libitum refeeding, calculated as the deviation in fat and FFM from their respective prestarvation values (ie, the amount of fat or FFM before ad libitum refeeding as a percentage of fat or FFM during the control period); and 3) the deficit in energy intake before ad libitum refeeding, calculated as the difference between the energy intake during the period of restricted refeeding and that during the control period. The results indicate that 1) the total hyperphagic response is inversely correlated with the degree of fat recovery (r = -0.6) as well as with that of FFM recovery (r = -0.5), 2) the correlation between hyperphagia and FFM recovery persists after adjustment for fat recovery, and 3) the correlations between hyperphagia and fat recovery or FFM recovery persist after adjustment for the variance in the energy deficit during the preceding period of restricted refeeding. Taken together, these results in humans suggest that poststarvation hyperphagia is determined to a large extent by autoregulatory feedback mechanisms from both fat and lean tissues. These findings, which have implications for both the treatment of obesity and for nutritional rehabilitation after malnutrition and cachexia, have been integrated into a compartmental model of autoregulation of body composition, and can be used to explain the phenomenon of poststarvation overshoot in body fat.
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PMID:Poststarvation hyperphagia and body fat overshooting in humans: a role for feedback signals from lean and fat tissues. 906 20

Tumor necrosis factor-alpha (TNF-alpha) is a cytokine involved in the physiological and metabolic abnormalities found in cachectic states. Until very recently, it was inconceivable to think of TNF-alpha in obesity. However, recent studies have shown that TNF-alpha can also play a key role in obesity, the cytokine being overexpressed in adipose tissue of obese rodents and humans. The aim of this review is to reconcile the role of TNF-alpha in these two opposite metabolic situations: obesity and cachexia. It is suggested that TNF-alpha may have a key role in the control of body mass in normal weight-controlled situations and that abnormalities in either its production (during cachexia) or action (during obesity) are responsible for the lack of control of body weight.
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PMID:Journey from cachexia to obesity by TNF. 927 59

The expression of leptin, an adipocyte-derived protein whose circulating levels reflect energy stores, can be induced by tumor necrosis factor (TNF)alpha in rodents, but an association between the TNF alpha system and leptin levels has not been reported in humans. To evaluate the potential association between serum leptin and the TNF alpha system, we measured the levels of soluble TNF alpha-receptor (sTNF alpha-R55), which has been validated as a sensitive indicator of activation of the TNF alpha system. We studied two groups: 1) 82 young healthy normal controls and 2) 48 patients with noninsulin dependent diabetes mellitus (NIDDM) and 24 appropriately matched controls. By simple regression analysis in controls, there was a strong positive association between leptin and 3 parameters: body mass index, sTNF alpha-R55, and insulin levels. In a multiple regression analysis model, leptin remained significantly and strongly associated with body mass index, and the association of leptin with both insulin and sTNF alpha-R55, although weakened, remained significant. Patients with NIDDM had leptin concentrations similar to controls of similar weight. Importantly, serum levels of sTNF alpha-R55 were also positively and independently associated with leptin in this group of diabetic subjects and matched controls. These data are consistent with the hypothesis that the TNF alpha system plays a role in regulating leptin levels in humans. Further elucidation of a possible role of the TNF alpha system in leptin expression and circulating levels may have important implications for our understanding of obesity and cachexia in humans.
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PMID:Leptin concentrations in relation to body mass index and the tumor necrosis factor-alpha system in humans. 932 77

Fuel metabolism generates signals that the brain uses to control food intake. Because the influence of metabolism on eating behavior depends on where and in what way metabolic fuels are utilized, the partitioning of fuels among different tissues and between metabolic pathways has significant effects on food intake. There is substantial evidence that shifts in fat fuel partitioning between oxidation and storage influence food intake, and data indicate that this may also be the case for carbohydrates. Carbohydrate and fat fuel interactions appear to affect eating behavior, and may play a role in the overconsumption of high-fat diets. A mechanism for the control of eating behavior that is sensitive to a stimulus generated at the level of oxidative phosphorylation and ATP production may underlie changes in food intake associated with shifts in fuel partitioning. A model based on such a mechanism provides a framework for understanding changes in food intake under a variety of conditions associated with alterations in energy storage and expenditure, including obesity and cachexia.
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PMID:Fuel partitioning and food intake. 949 62

Animals with cardiac disease can have a variety of nutritional alterations for which interventional nutrition can be beneficial. Deviation from optimal body weight, both obesity and cachexia, is a common problem in cardiac patients and adversely affects the animal. Methods for maintaining optimal weight are important for good quality of life in dogs and cats with cardiac disease. Providing proper diets to prevent excess intake of sodium and chloride also is important, but severe salt restriction may not be necessary until later stages of disease. Certain nutrient deficiencies may play a role in the pathogenesis or complications of cardiac disease, but nutrients also may have effects on cardiac disease which are above and beyond their nutritional effects (nutritional pharmacology). Supplementation of nutrients such as taurine, carnitine, coenzyme Q10, and omega-3 polyunsaturated fatty acids may have benefits in dogs or cats with cardiac disease through a number of different mechanisms. By addressing each of these areas maintaining optimal weight, avoiding nutritional deficiencies and excesses, and providing the benefits of nutritional pharmacology, optimal patient management can be achieved.
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PMID:Interventional nutrition for cardiac disease. 984 16


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