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

The activities of intestinal disaccharidases are known to be responsive to changes in the dietary intake of carbohydrates in the adult rat. Little is known, however, regarding the activities of these enzymes in obese subjects and how they are affected by differing carbohydrate intakes. To evaluate the effect of carbohydrate intake on the activity of intestinal disaccharidases in obesity, we used the genetically obese mouse C57BL/6J obob as an experimental model. Representing an example of early-onset obesity and mature-onset diabetes, this animal is characteristically hyperinsulinemic and hyperglycemic. Groups of obese mice and lean littermates were fed for 7 weeks equal amounts of either high-dextrose or low-dextrose isoenergetic diets. Sucrase, maltase, and lactase activities were measured on intestinal homogenates from the proximal and middle portions of the jejunoileum (upper and lower jejunum). Results were expressed as activity per tissue protein as well as total activity. Obese mice were found to have consistently greater total activity of both sucrase and maltase than their lean littermates, mostly as a result of increased intestinal size. Total lactase activity, however, was similar in the upper jejunum in both obese and lean mice, largely related to a decreased specific activity in obese mice. All mice fed the high-dextrose diet had significantly increased total activity of all disaccharidases studied when compared to the low-dextrose-fed animals, except for the lactase activity in the lower jejunum, where no differences were found in either group. Increases in activity related to high carbohydrate intake were a result of increases in specific activity.
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PMID:Effect of a high-dextrose diet on sucrase and lactase activity in jejunum of obese mice (C57BL/6J obob). 309 6

Electrolytic lesions of the ventromedial hypothalamus (VMH) produce an obesity syndrome characterized, in part, by excessive food intake and adiposity. Several hypotheses suggest that VMH lesion-induced hyperphagia results from elevated parasympathetic tone on the viscera expressed via the vagus nerves. To evaluate this possibility, vagally-mediated gastric acid secretion was measured in control and VMH-lesion rats. Initially, Pavlovian conditioning was used to elicit acid secretion to anticipated eating. VMH lesions eliminated the ability to mobilize acid secretion to the expectation of eating even though other behavioural indices of conditioning indicated that VMH rats still expected the food. The generality of the acid secretory deficit in VMH rats was evaluated by activating vagally-mediated acid secretion pharmacologically with insulin or 2-deoxy-D-glucose (2DG). VMH rats significantly increased acid secretion to insulin, although the response was attenuated compared to controls. Acid secretion stimulated by 2DG was normal. Thus the effects of VMH lesions on vagally-mediated acid secretion depend on the way in which the response is activated. The implications of this finding are discussed.
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PMID:Ventromedial hypothalamic lesions eliminate gastric acid secretion elicited by anticipated eating. 321 46

To examine the role of glucose transport proteins in cellular insulin resistance, we studied subcutaneous adipocytes isolated from lean control, obese control (body mass index [BMI] 33.4 +/- 0.9), and untreated obese non-insulin-dependent diabetes mellitus (NIDDM) patients (BMI 35.2 +/- 2.1; fasting glucose 269 +/- 20 mg/dl). Glucose transporters were measured in plasma membrane (PM), low-density (LDM), and high-density (HDM) microsomal subfractions from basal and maximally insulin-stimulated cells using the cytochalasin B binding assay, and normalized per milligram of membrane protein. In all subgroups, insulin led to an increase in PM glucose transporters and a corresponding depletion of transporters in the LDM. Insulin recruited 20% fewer transporters to the PM in the obese subgroup when compared with lean controls, and this was associated with a decline in LDM transporters with enlarging cell size in the control subjects. In NIDDM, PM, and LDM, transporters were decreased 50% in both basal and stimulated cells when compared with obese controls having similar mean adipocyte size. Cellular depletion of glucose transporters was not the only cause of insulin resistance, because the decrease in rates of [14C]-D-glucose transport (basal and insulin-stimulated) was greater than could be explained by reduced numbers of PM transporters in both NIDDM and obesity. In HDM, the number of transporters was not influenced by insulin and was similar in all subgroups. We conclude that (a) in NIDDM and obesity, both reduced numbers and impaired activity of glucose transporters contribute to cellular insulin resistance, and (b) in NIDDM, more profound cellular insulin resistance is associated primarily with a further depletion of cellular transporters.
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PMID:Role of glucose transporters in the cellular insulin resistance of type II non-insulin-dependent diabetes mellitus. 336 6

Rats with electrolytic or kainic acid (KA) lesions of the dorsomedial hypothalamic nucleus area (DMHA-L) are hypophagic, hypodipsic, and have a reduced body weight (BW) compared with controls. In the present study, male Sprague-Dawley rats received bilateral ibotenic acid (IBO) lesions of the DMHA (3 micrograms in 0.3 microliter) or sham (S) operations. During the next 32 days the IBO DMHA-L rats showed reduced (P less than 0.01) food and water intake, BW, and linear growth (P less than 0.03), although having a normal Lee obesity index. After a 24-h fast both groups became hyperphagic (P less than 0.01) with the DMHA-L group eating the most (P less than 0.01) during the 1st h; lost BW was regained at the same rate. In the absence of food, DMHA-L rats took less (P less than 0.01) water (data normalized) than S rats. During 24 h of water deprivation, both groups ate similar amounts of food (data normalized); following deprivation the groups were hyperdipsic. Both groups increased their food intake when given 300 mg/kg of 2-deoxy-D-glucose, which contrasts rats with electrolytic or KA DMHA-L rats. Both groups decreased their food intake when given cholecystokinin (3 micrograms/kg ip), which contrasts rats with electrolytic DMHA-L. The DMHA-L rats were not deficient in plasma glucose, insulin, growth hormone, or plasma Na+ and K+. Histology revealed many, but not all neurons, were destroyed in the DMN after IBO. The data indicate that IBO, electrolytic, or KA lesions of the DMHA produce similar but not identical physiological changes.
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PMID:Ingestive behavior of rats with ibotenic acid lesions of the dorsomedial hypothalamus. 357 58

Food additives continue to be a source of benefits to the consuming public but there are also perceived risks. Concern for the latter in the last decade has produced a society afflicted with cancer phobia. The intentional additives including sugars, salt, corn syrup, and dextrose make up 90% of the direct additives. These, along with a limited number of familiar items make up a large proportion of the remainder of the additives. Such common ingredients as nitrates and nitrites, solanine, cyanogenetic compounds, arsenic, etc., are unavoidably consumed in the diet and with little if any evidence for public health consequences. Major concern on the part of the public in recent years has been focused on man-made chemicals which are intentionally added to foods to enhance flavors and acceptability, nutrient value, shelf life and increased availability. These include food colors, nonnutritive and low-nutrient sweeteners, (saccharin, cyclamate, aspartame); antioxidants; and nitrites. Contaminants, sometimes incorrectly included in lists of food additives, present the greatest potential threat to public health. Such contaminants as mycotoxins, nitrosamines, polychlorinated biphenyls (PCBs), pesticides, among others, provide a continuing challenge to our regulatory agencies and to public health authorities. Evidence to date indicate that these responsible for food safety are doing an admirable job, and as a society, our food supply has never been better, or safer, and, as a population, we have never been healthier. Aside from contaminants, major concerns relate to an excess of good food and to obesity. These comments should not be taken to infer that we should relax our concern and surveillance; instead more concern and surveillance should be exerted toward those uncontrolled substances such as natural plant products and alleged natural nutrients, roots, herbs, etc., which are given much credit for positive health effects, without meeting the high standards of our legitimate food industry.
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PMID:Food additives and contaminants. An update. 375 9

The feeding responses induced by systemic administration of 2-deoxy-D-glucose (2-DG) and paraventricular hypothalamic injection of norepinephrine were assessed in Brattleboro rats deficient in vasopressin (VP). Controlling for the non-specific complications of diabetes insipidus, it was found that Brattleboro rats have a deficient 2-DG-feeding response, but an essentially normal noradrenergic-feeding response. Specific carbohydrate appetite abnormalities were also demonstrated. It is argued that VP influences 2-DG feeding by mobilizing endogenous energy stores following its acute release from the hypothalamoneurohypophysial system. A new function is thus ascribed for VP and the neural lobe of the pituitary. It is suggested that VP plays a role in stress-induced feeding and in specific aspects of carbohydrate appetite. The potential relevancy of vasopressin perturbations to bulimia nervosa and to the Prader-Willi obesity syndrome is also discussed.
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PMID:Vasopressin and glucoprivic-feeding behavior: a new perspective on an 'old' peptide. 377 90

A single systemic injection of bipiperidyl mustard (BPM) in the adult rat produces brain lesions and associated obesity without hyperphagia. To characterize some endocrine-metabolic aspects of the BPM preparation we measured plasma insulin and glucose dynamics as well as glucoprivic feeding. BPM-treated animals with verified lesions of the medial portion of the solitary tract nucleus (NTS) and the medial pole of the dorsal motor nucleus of the vagus (DMNX), as well as small lesions affecting the arcuate nucleus and basomedial portion of the ventromedial nucleus of the hypothalamus, showed the following characteristics: normal basal glycemia and insulinemia, exaggerated plasma insulin responses to oral or intravenous glucose and to oral saccharin, increased plasma glucose levels after oral glucose, unimpaired feeding to 2-deoxy-D-glucose challenge, decreased short-term intake of highly palatable food, and 36% more body fat at the end of the experiment. None of these changes occurred in rats that failed to develop lesions after BPM administration. These results suggest that BPM lesions (which appear to overlap distributions of central insulin binding sites) both affect a central mechanism controlling the pancreatic beta-cells and possibly influence gastric emptying and/or intestinal glucose absorption.
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PMID:Altered plasma insulin and glucose after obesity-producing bipiperidyl brain lesions. 388 85

The effect of several drugs on food intake has been examined in two strains of rats, one (S 5B/P1) which is resistant to developing obesity when eating a high fat diet, and one (Osborne-Mendel) which readily develops obesity when eating the same diet. Insulin and 2-deoxy-D-glucose increased food intake in a dose dependent manner in both S 5B/P1 and Osborne-Mendel rats. However, the S 5B/P1 rats showed a greater response, with a shorter latency period, to both agents than did the Osborne-Mendel rats. Conversely, d-amphetamine at the higher doses produced a dose dependent suppression of food intake with maximal suppression being similar for both strains. At a lower dose, however, d-amphetamine significantly increased food intake in the Osborne-Mendel rats, but not in the S 5B/P1 rats. The S 5B/P1 rats were also slightly more sensitive to the anorexic effects of lower dose adenosine than were the Osborne-Mendel rats whereas the reverse was true following higher dose adenosine. Naloxone suppressed food intake equally in both strains and D-glucose did not alter food intake in either strain. These studies identify three drugs, all stimulatory, to which the two strains of rat respond differently.
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PMID:Dietary obesity: effects of drugs on food intake in S 5B/P1 and Osborne-Mendel rats. 388 47

The effects of mazindol (MZD), a non-amphetaminergic anorectic agent, on the peripheral and central control of gastric acid secretion was investigated in rats. Gastric acid secretion induced by direct application of the muscarinic cholinergic agonist, carpronium, on parietal oxyntic cells was not affected by MZD. Secretion induced by 2-deoxy-D-glucose (2DG) was markedly suppressed by intra-hypothalamic or systemic (i.v.) administration of MZD; that induced by insulin was suppressed by systemic MZD. Electrophoretic application of MZD inhibited the neuronal activity of gastric and non-gastric type glucose sensitive neurons in the lateral hypothalamus (LHA), and excited glucoreceptor neurons in the ventromedial hypothalamus (VMH). The results suggest that previous reports of feeding suppression by MZD could be explained by its effects directly on hypothalamic feeding control neurons. This is consistent with the suggestion that it might be effective in the treatment of obesity.
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PMID:Effects of the non-amphetaminergic anorexiant, mazindol, on neuronal activity and hypothalamic control of gastric acid secretion in rats. 390 42

A dual isotope scintigraphic technique was used to assess the effect of increasing the caloric content of the liquid component of a mixed solid and liquid meal on gastric emptying in control and obese subjects. For the two test meals used gastric emptying of solid was significantly slower in the obese subjects compared to the control subjects. In both obese and control subjects the substitution of 25 per cent dextrose for water as the liquid component of the meal resulted in a significant delay of both solid and liquid emptying. The magnitude of this change was similar in obese and control subjects. The results suggest that the duodenal receptor mechanisms which slow gastric emptying are not defective in obesity.
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PMID:Effect of increasing the caloric/osmotic content of the liquid component of a mixed solid and liquid meal on gastric emptying in obese subjects. 395 11


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