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

Three cases of severe anorexia are reported. It results in a strong protein malabsorption with hepatic steatosis and in a syndrome of mental depression which needed the re-establishment of the intestinal-continuity. Although a mild post-operative anorexia is regular and contributes to the weight loss, massive anorexia must be considered as a new and redoubtable unpredictible complication of the surgical treatment for obesity, which may hinder the intestinal adaptation and increase the protein malabsorption.
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PMID:[Anorexia: a redoubtable complication of the surgical treatment for obesity after jejuno ileal by-pass (author's transl)]. 9 23

Plasma lipids and lipoproteins, glucose tolerance, plasma insulin response to glucose load, and liver function were examined in 81 relatives of 12 index cases with primary endogenous hypertriglyceridemia, hyperinsulinemia, and hepatic steatosis, as well as in 90 nonrelatives, including the spouses, as controls. Insulin hypersecretion (with or without glucose intolerance), endogenous hypertriglyceridemia, and abnormal liver function suggesting hepatic steatosis were shown to exist in the relatives mostly in combined fashion. Correlation analysis and stepwise multiple regression analysis revealed that the combined disorder developed on the basis of obesity. The incidence of diabetes mellitus was significantly high in the relatives (14.8 per cent) as compared with the normal Japanese population (3.5 per cent). Although the vertical transmission of the combined disorder was noted in almost all pedigrees, the frequency distribution analysis of insulin response, glucose tolerance, and plasma triglyceride showed the histograms of these variables similarly skewed to the right as compared with those of the controls, with no apparent bimodality. In view of the hitherto suggested role of insulin in triglyceride metabolism, it is concluded that hyperinsulinemia coupled with obesity seems to be the basic trait of this form of familial hypertriglyceridemia and hepatic steatosis, though the mode of transmission remains to be elucidated.
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PMID:Interactions of obesity and glucose-stimulated insulin secretion in familial hypertriglyceridemia. 65 14

In 40 obese patients, the liver function and the morphological picture were examined before and after jejuno-ileostomy. In 94% of the patients, distinct fatty liver was observed already before the small bowel exclusion, and the function tests showed an impaired function of this organ in 25% of the subjects before the operation. No clinical symptoms of liver insufficiency were recorded during the postoperative period. During one to three months after surgery, an increased impairment of the liver function was ascertained but, later on, a gradual improvement. More than one year after jejuno-ileostomy, the function test results were considerably better than before the operation. The degree of steatosis increased in the majority of the patients within 6 months after surgery, and some time later a considerable decrease in fatty liver was observed. Within 18 to 24 months after the jejunoileostomy, the morphological picture of the liver did not differe from the normal. The impaired function and the increased degree of steatosis were noted during diarrhea and rapid loss of body weight. The reson for this is most probably the protein malnutrition caused by the radical reduction in the absorption surface of the small bowel. The improved function and morphological picture of the liver are related to the progress of adaptation changes of the active part of small bowel. The results of the author's research do not confirm the hypothesis of permanent, harmful effect of jejuno-ileostomy on the state of the liver. The symptoms observed are definitely of a periodical and transient character, and are therefore not contra-indicated in the application of this operation in morbid extreme obesity treatment.
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PMID:Function and morphological picture of the liver in obese patients before and after jejunoileostomy. 74 72

Diabetes mellitus occurs in many animals species. However, only a few have been utilized in systematic studies designed to answer unsolved problems associated with the disorder in man such as molecular basis, pathogenesis of the vascular and neural lesions, and the roles of diet, exercise and obesity. Among the animal models available, rodents have been studied most thoroughly for a number of reasons: a) short generation time (sexually mature at about 3 mo of age, gestation time 21 days) and life-span is approximately 3 yr; b) hyperglycemia and/or obesity is known to be inherited in several species; c) environmental factors can be controlled easily in the laboratory because of small size; and d) economic considerations. The better-known rodent diabetes/obesity syndromes may be categorized as follows: 1) hyperglycemic with ketoacidosis, nonobese (Chinese hamster, South African hamster); 2) hyperglycemic with insulin hypersecretion, moderate obesity and may develop ketoacidosis (diabetic mouse (db/db), spiny mouse, sand rat); and 3) less pronounced hyperglycemia with hyperinsulinemia, insulin "resistance" and marked obesity (obese (ob/ob), yellow (Ay) and New Zealand obese (NZO) mice, and the Zucker "fatty" rat). The PBB/Ld mouse, described here in detail for the first time, is a new strain of mouse that also fits into the latter category. Members of this strain following maturity develop an obesity that is characterized by increasing cellularity of adipose tissue, increased serum immunoreactive insulin, reduced glucose tolerance, fatty liver, and hyperlipidemia. Therefore, this strain of mouse represents another model for study of adult onset obesity.
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PMID:Animal models of diabetes and obesity, including the PBB/Ld mouse. 77 Jan 97

A patient with liver dysfunction following small-bowel bypass for obesity was treated successfully with intravenous hyperalimentation. The hepatic steatosis and dysfunction were most likely caused by the preferential absorption of carbohydrate in the remaining small bowel, with resulting relative protein starvation. Routine use of high-protein, low-carbohydrate diets postoperatively until weight stabilization has occurred may prevent this complication.
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PMID:Liver dysfunction following small-bowel bypass for obesity. Nonoperative treatment of fatty metamorphosis with parenteral hyperalimentation. 81 54

A distict alcoholic withdrawal syndrome in chronic alcoholics cannot only be induced upon withdrawal of alcohol or dose reduction but also occurs upon continuous and long lasting consumption of larger quantities of alcohol. In the latter case we deal with an alcoholic predelirium which is characterized by simultaneous occurence of neurologic, vegetative and gastrointestinal disturbances as well as mental symptoms like anxiety, increased irritability and disturbance of sleep. In parallel to this alcoholic withdrawal syndrome from internal medical view a characteristic symptomatology can be observed in patients with chronic alcohol abuse. In most cases younger patients are concerned who, concomitantly with predelirant symptoms frequently display a labile hyperlipidemia and additional obesity, fatty liver, hyperlipidemia and often also hyperuricemia. Based on ten typical cases the combination of symptoms as described above is introduced. This combination can according to Feuerlein be defined as "alcohol-syndrome". The difficulties of diagnosis are shown because in many cases not the alcohol abuse but primarily vegetative and other functional disturbances dominate the clinical appearance. Additionally the pathogenetic connection between the described symptoms and alcohol abuse are discussed.
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PMID:[The "alcohol-syndrome" from internal medical view (author's transl)]. 86 89

The physical disease profiles of 135 female and 736 male inpatient alcoholics, similar in age, social class, and referral pattern, were compared to further clarify the widespread clinical impression that female alcoholics are more illness-prone. Although the women had been drinking hazardously for fewer years, at admission the prevalence of most diseases was similar in men and women. There was, however, an excess of anemia in women and of fatty liver and chronic obstructive lung disease in men. Furthermore, the average duration of hazardous drinking before the first recorded occurrence of almost all illness events was shorter in women, the sex differences being statistically significant for fatty liver, hypertension, obesity, anemia, malnutrition, gastrointestinal hemorrhage, and an ulcer requiring surgery. These findings suggest that the development of physical morbidity in relation to hazardous drinking may be accelerated in women.
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PMID:Morbidity in alcoholics. Evidence for accelerated development of physical disease in women. 87 27

The most serious adverse effect of standard intestinal bypass for obesity is the high incidence of hepatic dysfunction and death from hepatic failure. We therefore examined the long-term effects of a modified form of jejunoileal bypass (in which a greater continuous length of ileum is retained), on liver function in 120 patients. Substantial weight loss (119-0+/-SD 23-3 kg to 82-3+/-18-8 kg) occurred during the first nine months after surgery, accompanied by a significant rise in serum concentrations of bilirubin, alanine transferase, and alkaline phosphatase, and a significant reduction in albumin concentrations. Biochemical changes were unrelated to weight loss or halothane anaesthesia. After weight stabilisation liver function reverted to normal, and four years after bypass sulphobromophthalein retention and hepatic histology did not differ from those in obese controls. There were two postoperative deaths. Three other patients died during the period of rapid weight loss with severe hepatic steatosis. While transient mild impairment of liver function is common after modified jejunoileal bypass, clinically significant hepatic dysfunction is a rare and unexplained early complication.
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PMID:Hepatic structure and function after modified jejunoileal bypass surgery for obesity. 91 71

To evaluate the role of insulin in familial hypertriglyceridemia, 34 relatives of the pedigrees of 3 index cases of endogenous hypertriglyceridemia and hepatic steatosis as well as 9 spouses were examined for plasma lipids and responses of blood glucose and plasma insulin during oral glucose tolerance tests. The combined disorders of hypertriglyceridemia and hyperinsulinemia plus glucose intolerance--insulin resistance--were most commonly found among the relatives, which were often accompanied by an impaired liver function. Some relatives showed hyperinsulinemia without hypertriglyceridemia. Obesity was frequent, but its incidence was similar to the controls. Thus, the observed form of familial hypertriglyceridemia was apparently coupled with insulin resistance; and hyperinsulinemia, or insulin resistance by itself, might be a basic genetical trait in this form of lipid disorder.
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PMID:Evidence for a familial form of hypertriglyceridemia as disorders coupled with insulin resistance. 96 Jan 7

Marked fatty liver was found to develop in both KK and KK-Ay (yellow KK) mice when they were allowed free access to a 15% ethanol solution as drinking fluid. The present studies were undertaken to elucidate the characterization of the fatty liver and associated changes. Chemical analysis showed that accumulated lipids were mainly triglycerides, whose fatty acid composition was changed with increases in palmitoleic and oleic acids, indicating augmentation in endogenous lipogenesis. An accumulation of small fat droplets was histologically observed in centrolobular hepatocytes extending to perilobular zones. Among the tested mice of seven strains, only KK and KK-Ay mice developed the ethanol-induced fatty liver, and the latter mice were more susceptible. Growth, food and alcohol intakes, plasma levels of glucose, triglycerides, and immunoreactive insulin were also surveyed during the development of the alcoholic fatty liver. In contrast to high energy diet, ethanol induced neither development of obesity nor exaggeration of diabetic states. A possible correlation between the pathogenesis of the fatty liver and the genetic factor inherited in KK mice is discussed.
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PMID:Induction of fatty liver by ethanol drinking in KK and KK-Ay mice. 115 19


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