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Query: UMLS:C0497406 (overweight)
 26,365 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ethanol at an average blood concentration of 1 mg. per milliliter enhanced the immediate (first-phase) and prolonged (second-phase) insulin response to an intravenous glucose load in nonfasting normal human subjects. Simultaneously, the glucose disposal rate was increased and the postglucose hypoglycemia was accentuated, resulting in definite hypoglycemic symptoms in some individuals. Oral glucose tolerance was not changed by ethanol administration, but the thirty-minute blood glucose and plasma insulin values were increased, suggesting that alcohol might accelerate the absorption of glucose from the gut. Ethanol given orally during evening hours (1.5 gm. per kilogram) caused a nocturnal hyperinsulinemia and a decrease of blood glucose, but not an actual hypoglycemia. Oral glucose tolerance and plasma insulin response tested the next morning, when ethanol had disappeared from the blood, were not influenced by drinking the previous evening. The K-value of intravenous glucose was increased at this time, however. When alcohol was administered for one week at a dose corresponding to 25 per cent of daily calories and substituting for fat, both the oral and intravenous glucose tolerances were impaired in each subject but the insulin response remained unchaged. In obese nondiabetic subjects, ethanol did not potentiate the early insulin response to intravenous glucose but it increased the second phase of insulin secretion in response to sustained hyperglycemia. In contrast to conditions in nonobese subjects, the glucose disposal rate was not incresed and postglucose hypoglycemia was not accentuated by ethanol in overweight subjects. In insulin-deficient diabetic patients the absent early insulin response could not be restored by ethanol, and the late component of insulin release was little increased by alcohol infusion. Ethanol did not improve the glucose utilization of diabetic patients.
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PMID:Ethanol-induced alterations of glucose tolerance, postglucose hypoglycemia, and insulin secretion in normal, obese, and diabetic subjects. 110 Apr 61

Several studies report that placenta and amniotic fluid (AF) may be a source of many peptide hormones. Although the presence of gastric inhibitory polypeptide (GIP) in amniotic fluid has not been described, it is present in the fetal gut. In this study we report the presence of insulin and GIP in human AF of normal and diabetic pregnancies. GIP concentrations in the AF collected two hours after an arginine tolerance test (ATT), at 34-36 weeks of gestation, were evaluated in 8 normal and 53 diabetic pregnant women. GIP was found in all samples of AF. The mean AF-GIP concentrations were 133 +/- 19 pmol/l in controls and 111 +/- 6 pmol/l in the diabetics, being the GIP values of the diabetics belonging to White Class B significantly lower than those of normals (99 +/- 10 vs 133 +/- 19 pmol/l). The GIP/IRI molar ratio was significantly lower in the diabetics than in controls (1.2 +/- 0.2 vs 2.5 +/- 0.4); moreover the GIP/IRI molar ratio was significantly higher in AF collected from diabetic pregnant women who delivered overweight infants than in AF of normal weight infants or controls. This finding would suggest a negative feedback mechanism between GIP and insulin in fetus.
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PMID:Gastric inhibitory polypeptide (GIP) concentration in human amniotic fluid. 389 70

The responses of gastric inhibitory polypeptides (GIP), gut glucagon-like-immunoreactivity (gut GLI), insulin, and pancreatic glucagon to a 50-g oral glucose load were studied in late pregnancy and postpartum in 11 normal women, 10 normal weight gestational diabetics, and 10 overweight gestational diabetics. The GIP response to glucose was impaired in pregnancy in all three groups. In pregnancy, the GIP response was smaller in both groups of gestational diabetics than in normal women, whereas postpartum, the GIP response was lower than normal in the normal weight gestational diabetics only. In pregnancy, the gut GLI response to glucose was reduced in the overweight gestational diabetics and abolished in the normal women. The insulin response to glucose was increased in pregnancy in all three groups. Moreover, it was higher in the overweight gestational diabetics than in the other two groups in pregnancy and postpartum. In the normals, the suppression of glucagon levels after glucose ingestion was more marked in pregnancy than postpartum, whereas no such effect was seen in gestational-diabetic pregnancy. It is concluded that pregnancy--normal as well as gestational-diabetic--is accompanied by profound changes in the secretion of gastrointestinal insulinotropic hormones after glucose ingestion. These findings may be important for the understanding of changes in metabolism and gastrointestinal physiology in gestation.
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PMID:Gastrointestinal insulinotropic hormones in normal and gestational-diabetic pregnancy: response to oral glucose. 701 14

The gastro-entero-pancreatic (GEP) hormone response to glucose ingestion is considerably altered in pregnancy in normal women and gestational diabetics. In normal women, also the GEP hormone response to protein is changed in pregnancy. In the present investigation, the gastrin, gastric inhibitory polypeptide (GIP), gut glucagon-like-immunoreactivity (gut GLI), insulin, pancreatic glucagon, and pancreatic polypeptide (PP) responses to a protein rich meal in pregnancy and postpartum were studied in 10 women with gestational diabetes. Five of the women were overweight and five were normal weight. Fasting and postprandial gut GLI and PP levels were reduced and insulin levels enhanced in pregnancy. No effect of pregnancy on fasting or postprandial gastrin, GIP, or glucagon levels was found. In pregnancy as well as postpartum, insulin levels were higher in the overweight than in the normal weight patients, whereas the concentrations of the other hormones were similar in the two subgroups of gestational diabetics. It is concluded that the GEP hormone response to a protein rich meal is influenced by late pregnancy in gestational diabetics in the same way as in normal women. The physiological consequences of the findings are not known in detail as yet but they may be important to carbohydrate metabolism and gastrointestinal physiology in pregnancy.
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PMID:Gastro-entero-pancreatic hormones in gestational diabetes: response to a protein rich meal. 711 58

Cimetidine reduces the appetite and weight in healthy overweight subjects. Gastrointestinal regulatory peptides such as cholecystokinin (CCK) have been proposed to mediate the satiety signal from gut to brain. Therefore, the effect of cimetidine on basal and postprandial plasma concentrations of cholecystokinin and gastrin was studied. After an overnight fast, 12 healthy volunteers were given cimetidine (400 mg) on day 1, breakfast on day 2, and cimetidine 20 min before breakfast on day 3. Plasma concentrations of cholecystokinin and gastrin were measured by radioimmunoassay. Plasma cholecystokinin concentration increased with one major peak observed 30 min and one smaller peak observed 120 min after intake of cimetidine. The meal induced an increase in the plasma concentration of cholecystokinin, while cimetidine prior to the meal elicited a sustained postprandial cholecystokinin response. Cimetidine had no effect on the basal plasma concentration of gastrin. The meal induced an increase in the plasma concentration of gastrin, while cimetidine prior to the meal elicited a sustained postprandial gastrin response. In conclusion, cimetidine increases the basal concentration of plasma cholecystokinin and elicits a sustained postprandial response of both cholecystokinin and gastrin. At least the cholecystokinin response may be one mechanism by which cimetidine reduces the appetite.
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PMID:Effect of cimetidine on basal and postprandial plasma concentrations of cholecystokinin and gastrin in humans. 914 53

The regulation of body fat stores is a problem of energy and nutrient balance that can be most readily viewed as a feedback system. Several elements are involved in any feedback system, including afferent signals, a controller that senses the afferent signals and transduces their information and then activates efferent controls that regulate the controlled system. The recent discovery of leptin has provided a major missing link in the feedback control system. This afferent signal is produced exclusively in fat cells of nonpregnant mammals but can be produced in the placenta as well. This circulating peptide has a very strong relationship to the level of body fat and its absence experimentally and clinically produces massive obesity. In the controller, or brain, several anatomic regions play a central role in regulating fat stores. Damage to the ventromedial nucleus (VMH) or the paraventricular nucleus (PVN) in the hypothalamus produces massive obesity in mammals and birds. Injury to the central nucleus of the amygala will also produce obesity. In contrast, damage to the lateral hypothalamus reduces body fat. The syndrome of leptin deficiency or defects in the leptin receptors produce a massive obesity that is metabolically similar to the VMH or PVN lesion syndromes of obesity, suggesting that leptin may have its metabolic effects through these medial hypothalamic centers. Support for this idea has come from studies showing that damage to the PVN or VMH will block the effects of leptin. A number of neuropeptides and monoamines are involved with modulating of food intake and fat stores. Both serotonin, acting through 5-HT2C receptors, and norepinephrine, acting through beta 2 and/or beta 3 receptors, reduce food intake. A variety of peptides also influence food intake and body fat. Neuropeptide Y, dynorphin, galanin, and melanocyte-stimulating hormone all increase food intake. In contrast, a large number of peptides--including cholecystokinin, corticotrophin-releasing hormone/urocortin, enterostatin, insulin, leptin, alpha-MSH, and TRH--reduce food intake. Chronic administration of neuropeptide Y, acting through Y-5 receptors, can produce chronically increased food intake and obesity. This syndrome is similar to the VMH syndrome and suggests that NPY must be acting as an inhibitor of a feeding system. The melanocortin receptor system may be particularly important because a mouse that does not express MC4 receptors is massively overweight. These central systems modulate food intake and fat stores by the controlled system. Glucocorticoids from the adrenal gland are important in obesity, since adrenalectomy will reverse or prevent the development of all forms of obesity. The sympathetic nervous system is also important because low sympathetic activity is associated with experimental and clinical obesity. The reciprocal relationship between food intake and sympathetic activity has been a robust relationship, suggesting that beta receptors in the periphery or brain may be involved in feeding control. In one model of dietary obesity resulting when animals eat a high-fat diet, the syndrome is blocked by inhibitory adrenal steroid activity. These animals show a lower level of sympathetic activity and a low level of brain serotonin. Finally, they show an enhanced sensitivity to essential fatty acids when these are applied to the tongue or given into the gut. In this chapter, the control of energy stores as fat is viewed as a feedback system. Leptin is perceived as a key afferent signal and glucocorticoids and the sympathetic nervous system through beta receptors as essential elements of this control system.
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PMID:The MONA LISA hypothesis in the time of leptin. 976 5

This review explains and surveys very recent findings and experimental results concerning molecular pathology and genetics of overweight and obesity and also evaluates their relevance for the actual treatment of obesity at present. Most of these studies were done on inbred obese mice or rats and it is yet unknown to what extent the results do apply to human overweight. Nevertheless these studies led to the discovery of a new hormone--OB-protein or leptin--produced by adipocytes of animals. It does not only increase satiety by influencing feeding centers and decrease body weight but it also interferes with several peripheral metabolic functions. Mutations of leptin expression or expression of leptin receptors as observed in animals are, however, very rare in humans. In obese individuals (and animals) there is a yet unexplained resistance to the effects of leptin which interferes with successful therapeutic use of leptin in human obesity. Various other recently discovered transmitters modifying feeding habits may, however, become targets of future drugs making dietary weight loss and its maintenance more acceptable and successful. At present obese people and patients have to rely, however, on traditional methods of weight loss though these are known to yield poor results over prolonged periods of time. Orlistat, a recently introduced drug results in malabsorption of fat from the gut by inhibiting lipases. Though it is not based on recent insights to regulation of body weight it is promising primarily for educating patients to reduce their nutritional fat intake.
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PMID:[New knowledge about obesity--news for obese patients?]. 987 83

RW94 is a naturally occurring common inorganic substance and a permitted additive in the food industry which binds to and precipitates free fatty acids in vitro. Our preliminary clinical trial showed a statistically significant increase in the quantity of faecal fat excreted by volunteers who had consumed RW94, showing that the fatty acids were also precipitated and not absorbed in vivo. It is therefore anticipated that RW94 will aid weight loss by preventing the absorption of some of the dietary fat. Five grams of RW94 were administered orally after each main meal to half of a group of 32 overweight or obese, but otherwise healthy, volunteers, the others receiving a placebo of maize starch. There was a statistically significant (p < 0.05) reduction in the mean weights of the RW94 group relative to their controls at three weeks, and this reduction was maintained throughout the remainder of the six-week trial period. In accordance with our previous findings, there was a higher incidence of abdominal discomfort, rumbling stomach and flatulence among the RW94 group, reflecting the possible transient changes in the bacterial ecosystem of the lower gut in response to the increased delivery of nutrients. These adverse events diminished as the bacteria apparently re-established equilibrium. It appears that the incidence of abdominal discomfort in its various forms following consumption of RW94 is lower than that initially indicated in the preliminary study. Thus, this second clinical trial performed under conditions approximating to the 'real life' situation confirmed that RW94 appears to help reduce the increase in weight following the consumption of excessive dietary fat without undue discomfort or inconvenience from adverse sequellae.
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PMID:A double-blind, placebo-controlled evaluation of the effects of RW94 on the body weight of both overweight and obese healthy volunteers. 989 Nov 97

Females have a greater susceptibility to ethanol-induced liver injury than males. Females who drink ethanol regularly and have been overweight for 10 years or more are at greater risk for both hepatitis and cirrhosis than males, and females develop ethanol-induced liver injury more rapidly and with less ethanol than males. Female rats on an enteral ethanol protocol exhibit injury more quickly than males and have widespread fatty changes over a larger portion of the liver lobule. Moreover, levels of plasma endotoxin, intracellular adhesion molecule-1, free radical adducts, infiltrating neutrophils and nuclear factor kappa B are doubled in female rat livers compared with male rat livers after enteral ethanol treatment. Additionally, estrogen treatment in vivo increases the sensitivity of hepatic macrophages or Kupffer cells to endotoxin. Evidence has been presented that Kupffer cells are pivotal in the development of ethanol-induced liver injury. Destroying Kupffer cells with gadolinium chloride or decreasing bacterial endotoxin by sterilizing the gut with antibiotics inhibits early inflammation due to ethanol. Similar results have been obtained with anti-tumour necrosis factor-alpha antibody. These data pointed to the hypothesis that ethanol-induced liver injury involves elevations in circulating endotoxin concentrations leading to activation of Kupffer cells, which causes a hypoxia-reoxygenation injury. This theory has been tested using pimonidazole, a 2-nitroimidazole marker, to quantify hypoxia in downstream, pericentral regions of the hepatic lobule. After chronic enteral ethanol treatment, pimonidazole binding doubles. Enteral ethanol also increases free radicals detected with electron spin resonance. Radical adducts, with coupling constants such as alpha-hydroxyethyl radical, have been shown to arise from ethanol. Importantly, hypoxia and radical production detected in bile are also decreased by the destruction of Kupffer cells with gadolinium chloride. These data support the hypothesis that Kupffer cells contribute to the vital sex differences in liver injury caused by ethanol.
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PMID:Sex-related liver injury due to alcohol involves activation of Kupffer cells by endotoxin. 1111 Jun 25

An analysis of a 121-day of intensive-care therapy of peritonitis and concomitant complications in a patient with Pickwick syndrome and somnolent apnea syndrome is reported. Right hemicolectomy was implemented in the patient for peritonitis, which developed on the 2nd day as a result of perforation of the blind gut at a place of tumor removed in a scheduled colonofibroscopy (CFS). The attempts of intubation of the trachea for as long as one hour failed due to the anatomic peculiarities. Tracheostomy was made. The switching-on of the patient, postoperatively, to spontaneous breathing was highly complicated because of Pickwick syndrome and the appearing dependence in the patient on the respirator. The alternating methods of respiratory support by using apparatus "Servo Ventilator 900" (Vo. Control + PEEP, SIMV, PS, regime CPAP) were a key technique of intensive care during 121 days. The postoperative cause was complicated on the 12th postoperative day by a massive gastrointestinal hemorrhage, by subsequent relaparotomy and a revision of anastomosis. The intensive-care therapy enabled, on the 80th day to transfer the patient, for 3 days, to a spontaneous independent breathing and to feed him, for 2 weeks, in the natural way. The subsequent postoperative cause was complicated by the development of massive decubituses in the lumbosacral area, and by the formation of intestinal fistula with leakages phlegmon in the anterior abdominal wall. The average cost of one day of the complex intensive-care therapy topped 5000 rubles. Because of an overweight (190 kg) the medical care rendered to the patient was complicated. The patient died on the 121 day due to intoxication, renal insufficiency and growing respiratory insufficiency. Finally, it is concluded that there is a necessity to make a motivated collective decision for carrying out any diagnostic invasive methods of examination in such category of patients; and in case of surgical interventions, the intubation of the trachea should be implemented with local spray anesthesia involving the use of fibrolaryngoscope.
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PMID:[Pickwick syndrome--problems for a surgeon and an anesthesiologist-resuscitator (clinical observation--121 days of intensive care of the patient with Pickwick syndrome)]. 1293 48


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