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

Results of CT and US examinations in 24 patients with testicular tumors yielded similar sensitivity and specificity in the diagnosis of enlarged retroperitoneal lymph nodes found at laparatomy. Therefore, the choice of either imaging modality may be influenced by other factors such as presence of abundant bowel gas, post-operative wounds, surgical clips in the abdomen, cachexia or obesity.
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PMID:Evaluation of retroperitoneum with computerized tomography and ultrasonography in patients with testicular tumors. 48 90

In cats and dogs, total duodenectomy with transplantation of the papilla Vateri into the jejunum and gastroenteroanastomosis has been shown to result in the so-called "duodenal deficiency syndrome" which is characterized, in the first phase, by cachexia of the animals occurring within 6 weeks after operation followed by obesity in the second phase. In contrast, animals with preserved by isolated duodenum do not exhibit pronounced changes in body weight as compared to intact controls. Consequently, it is suggested that intestinal hormones (enterines) not only exert gastrointestinal effects but also systemic ones. Thus, duodenectomy has been shown to lead to disturbances of lipid and protein metabolism, decreased secretory activities of the thyroid gland and the hypothalamus. Due to these findings, -- in addition to the even well-known intestinal hormones -- the existence of enterines with thyrotropic, lipotropic, hypothalamotropic, and appetite-regulating functions can be assumed which may make the duodenum act as an "abdominal hypophysis".
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PMID:Non-digestive functions of the intestinal hormones (enterines). New data and hypotheses based on experimental duodenectomy (Short review). 110 2

This review describes a homeostatic model for the regulation of nutrient intake and the control of partitioning between fat and protein storage. With this homeostatic model, the clinical abnormalities of energy storage such as obesity, anorexia nervosa, and cancer cachexia are examined and potential mechanisms suggested.
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PMID:Weight homeostasis. 203 67

The concept that hormonal substances can alter the expression of entire developmental programs is in itself not particularly new. The ability to define conditions under which a specific hormone can precociously activate the differentiation of a well-defined population of cells and under which another hormone can both block and reverse such a developmental progression, however, provides a major step forward toward unraveling the biochemical events that define the transition from a committed precursor to a fully differentiated cell. Further analysis of the molecular events initiated by glucocorticoids and TNF should provide insights into the control of adipogenesis and may generate a foundation for understanding the mechanisms by which other cells enter a particular differentiative lineage. In a more applied sense, such knowledge may also provide a rational approach to controlling metabolic disease syndromes related to adipogenesis gone awry such as obesity-associated diabetes and cachexia.
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PMID:Hormonal control of adipogenesis. 354 48

The highest incidence of defective wound healing in all surgical disciplines is observed after urological operations. Wound infections occur in more than 8% of all urological patients. Defective wound healing appears in about 17% of unselected nephrectomy cases, rising to 50% when pyonephrosis is present. Simple adenomectomy is associated with wound infection rates of between 8 and 12% in preoperatively uninfected patients and up to 50% in patients with preoperative bacteriuria. Numerous factors may influence wound healing, e.g. age, obesity, cachexia, chronic infectious and non-infectious diseases, anaemia, thrombopathy, faulty asepsis and antisepsis, preoperative showering and shaving, skin preparation, hand degerming, skin draping, duration of hospitalization, traumatic operative technique, suture material, diathermy, timing and length of operation, duration of hospitalization, and antibiotic regimen. Strict attention has to be paid to these factors if the incidence of postoperative wound infection is to be kept within reasonable limits.
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PMID:[Bacterial nosocomial infections in urology: defective wound healing]. 618 18

This report analyzes two kinds of studies of human energy balance; direct and indirect calorimetry for 24-hr periods, and complete measurements of food intake, waste, and tissue storage for 3 weeks and longer. Equations of energy balance are written to show that the daily quantity of metabolic energy, QM, is coupled with an unidentified quantity of unmeasured energy, QX, in order to make the equation balance. The equations challenge the assumed equivalence of direct and indirect calorimetry. The analysis takes the form of employing experimental data to calculate values for the arguable quantity, QX. Studies employing 24-hr direct calorimetry, 202 complete days, show that when food intake nearly matches QM, values for QX are small and probably insignificant, but when there is a large food deficit, large positive values for QX appear. Calculations are also made from studies of nutrient balance during prolonged overeating and undereating, and in nearly all cases there were large negative values for QX. In 52 sets of data from studies lasting 3 weeks or longer, where all the terms in the balance equation except QX were either directly measured or could be readily estimated, the average value for QX amounts to 705 kcal/day, or 27% of QM. A discussion of the nature of QX considers error and the noninclusion of small quantities like the energy of combustible gases, which are not thought to be sufficient to explain QX. It might represent the cost of mobilizing stored fuel, or of storing excess fuel, or it might represent a change in internal energy other than fuel stores, but none of these is thought to be likely. Finally, it is emphasized that entropy exchange in man as an open thermodynamic system is not presently included in the equations of energy balance, and perhaps it must be, even though it is not directly measurable. The significance of unmeasured energy is considered in light of the poor control of obesity, of the inability to predict weight change during prolonged diet restriction or intentional overeating, and of the energetics of tissue gain in growth and loss in cachexia. It is not even well established how much food man requires to maintain constant weight. New studies as they are undertaken should try to account completely for all the possible terms of energy exchange.
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PMID:The measurement of energy exchange in man: an analysis. 738 17

Nonalcohol-induced fatty liver is widely believed to be a benign condition with little or no risk of disease progression. There have been occasional reports of progression to cirrhosis but none in the absence of preexisting fibrosis on the index biopsy specimen even when co-existing hepatitis was present (steatohepatitis). From our histological database (1978 to 1985), we identified 161 patients with fatty liver seen at our institution and traced the case notes of 156. One hundred five patients were initially excluded as having an alcohol-induced cause, and the remaining 51 either were seen in the clinic (37) or had died, in which cases copies of their death certificates were obtained (14). A further 7 patients were excluded after clinic attendance gave evidence of alcohol excess and another 4 after review of their initial biopsy showed the presence of fibrosis or steatohepatitis. The apparent cause of the steatosis in the 40 included patients with strictly nonalcohol-induced pure fatty liver was obesity in 12, diabetes in 4 (1 obese patient), and cachexia associated with extrahepatic malignancy in 6. Four of the remaining 19 had serological evidence of an autoimmune disorder, but none of these had any clinical or histological features of autoimmune liver disease. Nine patients had evidence of hyperlipidemia, 3 of whom were also obese. At a median follow-up of 11 years (7 to 16), 12 of 26 living patients had abnormal results of liver blood tests and had repeat liver biopsies performed. None had progressed to steatohepatitis or cirrhosis; 1 obese patient had developed mild fibrosis 9.8 years after her index biopsy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The natural history of nonalcoholic fatty liver: a follow-up study. 748 79

Tumor necrosis factor-alpha (TNF) has been suggested to be the mediator of insulin resistance in infection, tumor cachexia, and obesity. We have previously shown that TNF diminishes insulin-induced tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1). The current work examines potential mechanisms that mediate this event. TNF effect on IRS-1 in Fao hepatoma cells was not associated with a significant reduction in insulin receptor tyrosine kinase activity as measured in vitro but impaired the association of IRS-1 with phosphatidylinositol 3-kinase, localizing TNF impact to IRS-1. TNF did not increase protein-tyrosine phosphatase activity and protein-tyrosine phosphatase inhibition by vanadate did not change TNF effect on IRS-1 tyrosine phosphorylation, suggesting that protein-tyrosine phosphatases are not involved in this TNF effect. In contrast, TNF increased IRS-1 phosphorylation on serine residues, leading to a decrease in its electrophoretic mobility. TNF effect on IRS-1 tyrosine phosphorylation was not abolished by inhibiting protein kinase C using staurosporine, while inactivation of Ser/Thr phosphatases by calyculin A and okadaic acid mimicked it. Our data suggest that TNF induces serine phosphorylation of IRS-1 through inhibition of serine phosphatases or activation of serine kinases other than protein kinase C. This increased serine phosphorylation interferes with insulin-induced tyrosine phosphorylation of IRS-1 and impairs insulin action.
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PMID:Tumor necrosis factor alpha-induced phosphorylation of insulin receptor substrate-1 (IRS-1). Possible mechanism for suppression of insulin-stimulated tyrosine phosphorylation of IRS-1. 755 52

Tumor necrosis factor-alpha (TNF alpha) is a cytokine implicated in the development of septic shock, cachexia, and other pathological states. Recent studies indicated a direct role for adipose expression of TNF alpha in obesity-linked insulin resistance and diabetes. Pioglitazone, CP-86,325 (CP), AD-5075, CS-045, ciglitazone, and englitazone are members of a new class of insulin-sensitizing thiazolidinedione derivatives with in vivo antidiabetic activities. To test whether these agents antagonize the effect of TNF alpha, 3T3-L1 cells were induced to differentiate in the presence of TNF alpha with or without thiazolidinedione derivatives. Incubation of 3T3-L1 cells with TNF alpha alone completely inhibited adipocyte conversion and expression of fatty acid-binding protein messenger RNA (mRNA). However, coincubation of TNF alpha-treated cells with CP (1 microM), AD-5075 (1 microM), pioglitazone (10 microM), or CS-045 (10 microM) blocked these effects. Long term incubation of 3T3-L1 adipocytes with a low dose of TNF alpha (50 pM) significantly decreased the levels of the adipocyte/muscle-specific glucose transporter (GLUT4) and the CCAAT enhancer-binding protein mRNAs, but did not affect expression of the ubiquitously expressed glucose transporter (GLUT1) or lipoprotein lipase mRNAs. Incubation of 3T3-L1 adipocytes with TNF alpha also inhibited insulin-stimulated 2-deoxyglucose uptake as well as expression of GLUT4 protein. Furthermore, in 3T3-L1 adipocytes, incubation with TNF alpha attenuated the expression of fatty acid-binding protein mRNA in a time- and dose-dependent manner. These inhibitory effects were partially or completely blocked by coincubation of the cells with CP. These results implicate that the insulin-sensitizing agents may exert their antidiabetic activities by antagonizing the inhibitory effects of TNF alpha.
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PMID:Antidiabetic thiazolidinediones block the inhibitory effect of tumor necrosis factor-alpha on differentiation, insulin-stimulated glucose uptake, and gene expression in 3T3-L1 cells. 789 57

Adipsin, which is identical to complement factor D, is synthesized by fat cells, circulates in the bloodstream and is profoundly deficient in mice with genetic and hypothalamic obesity. With the recent cloning of human adipsin, a quantitative human immunoassay has been developed. In the present study, we measured adipsin blood concentrations in humans with increased and decreased adipose stores as well as adipsin secretion by adipose tissue obtained from lean and obese individuals. The results demonstrate that adipsin is released by human adipose tissue fragments as has previously been shown in mice, and that, in contrast to obese mice, blood adipsin concentrations were not reduced in the obese humans tested in this study. We also observed that blood adipsin concentrations can vary as a function of feeding or adiposity, in that they tend to be mildly elevated in obese individuals or mildly reduced in individuals with total lipo-atrophy, cachexia related to AIDS and anorexia nervosa. Thus, the circulating concentration of adipsin tends to correlate positively with degree of adiposity. Clearly, no deficiency in blood adipsin concentrations or adipsin secretion by adipose tissue was observed in the obese individuals studied.
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PMID:Concentrations of adipsin in blood and rates of adipsin secretion by adipose tissue in humans with normal, elevated and diminished adipose tissue mass. 804 95


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