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Query: UMLS:C0028754 (obesity)
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The objective of this paper is to characterize the fat cow syndrome. This condition refers to a combination of metabolic, digestive, infectious, and reproductive conditions which affects the obese periparturient cow. The condition develops primarily due to faulty feed management which permits excessive consumption of unbalanced diets. The syndrome is frequently a herd problem characterized by a high morbidity and mortality due to an increase in disease in periparturient cows. Clinical signs include depression, anorexia, ketonuria, marked decrease in production, progressive debilitation, weakness, nervous signs, and an elevation in temperature due to infectious disease. The obesity is generalized throughout the body with extensive fatty metamorphosis in the liver. Histological changes are primarily in the liver and kidney. Treatment of the condition consists of feeding a balanced diet, symptomatic treatment, and good supportive care. The condition can be prevented by feeding a balanced diet according to nutrient requirements of the National Research Council.
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PMID:Fat cow syndrome. 96 40

Effects of a 24 hour fast were studied in 21 obese children aged 7 to 14 and in 8 controls. Mean blood glucose (BG) during fast dropped more in controls (0.88 to 0.54 g/l) than in obese (0.90 to 0.63 g/l) Plasma cortisol changes were similar in the 2 groups, FFA increased (p less than 0.01) in the 2 groups, but the 24 hour mean level was higher in controls (4.0 mEq/l) than in obese (2.06 mEq/l). At the end of the fast, a ketonuria was present in all obese children except 2. Serum alanine dropped similarly in obese (28 to 24 muM p. cent ml) and in controls (30 to 22 muM p. cent ml). All obese exhibited at the end of the fast a significant rise (p less than 0.01) of branched chain aminoacids, not observed in controls. Responses to glucagon (0.03 mg/kg I.M.) were studied before and after fast. At time 0, BG response was higher and more prolonged in obese in spite of hyperinsulinism. At time 24 hours, BG raised from 0.50 to 0.74 g/1 and insulin from 8 to 35 muU/ml in controls, while in obese BG raised from 0.63 to 1.06 g/l and insulin from 25 to 88 muU/ml. Concomitant hyperinsulinsim and biological criteria of hypoinsulinism demonstrated in obese children the peripheral resistance to insulin. The contrast between a normal degree of protein gluconeogenesis and a reduced rate of fat mobilization during fast may be a major biological feature of obesity in childhood.
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PMID:Effect of 24 hour fast in obese children. 100 33

Sanatorium treatment for 27 days was carried out for 52 patients with obesity of alimentary metabolism type, consisting of moderate loading and high-protein, high-lipid diet with 2430 to 2840 cal daily, with unusually low carbohydrate contents--10 g for the first week and 38 g--in the fourth. The authors established a favourable total and an average daily body weight loss of the patients, irrespectively of the relatively high caloric intake. No sense of hunger was reported from the majority of the patients. The subjective complaints observed are more frequent and more severe, as compared with the other treatment regimens with reducing but balanced dietetic regimens. The majority of the subjective complaints established could be associated with the objectively confirmed compensated metabolic ketoacidosis. The unfavourable changes in the followed-up laboratory indices are: considerable decrease of blood sugar, massive ketonuria, elevation of serum uric acid and deviations in the acid-base parameters. Serum lipid indices fell under the effect of the treatment and body weight reduction. What impresses is the serum cholesterol reduction in spite of the high exogenic import, the diminution of cholesterol-lecithin index and the marked elevation of free fatty acid in serum, manifestation of incresed lipolysis in the lipid depots. (he diet indicated is not balanced and not physiological. It must be applied casually in obesity treatment. Its application is possible only after a strict assessment of each individual patient with obesity with no accompanying diseases, that do not agree with the partial fasting and cannot be included in intensive motor regimen.
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PMID:[Treatment of obesity with a high-protein, high-fat, "carbohydrate-free" diet]. 101 11

Whereas short-term cold exposure depletes glycogen reserves, repeated and prolonged moderate exercise in a cold environment creates an energy deficit that is satisfied by an increased metabolism of depot fat. Factors contributing to the fat loss include an exercise-induced hypertrophy of lean tissue, a loss of energy through a cold-induced ketonuria, a stimulation of resting metabolism, increases in the energy cost of movement, and a lower yield of energy per litre of oxygen consumed. Biochemical explanations of the enhanced lipolysis include increased catecholamine secretion, altered sensitivity of catecholamine receptors, and decreases of circulating insulin. The enhanced fat loss with combinations of cold and exercise may be helpful in the therapy of obesity, although the response seems less well developed in women than in men. Moreover, there may be other objections to cold exposure in an older obese population. Short-term glycogen depletion has negative implications for the endurance competitor. Cold acclimation, by favoring an insulative response to cold, reduces glycogen depletion; endurance training may supplement this effect by enhancing the activity of fat-metabolizing enzymes.
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PMID:Fat metabolism, exercise, and the cold. 132 16

Calorie restriction is widely used as a primary therapy for obese pregnant women with gestational diabetes. To better understand the metabolic consequences of marked calorie restriction, we performed a randomized prospective trial under metabolic ward conditions. Obese gestationally diabetic women were randomized to control (n = 5) and calorie-restricted (n = 7) groups. All patients consumed an approximately 2400-kcal/day diet during the 1st wk of the study, and at the end of the 1st wk, metabolic features of the two groups were statistically indistinguishable. During the 2nd wk, the control group continued to consume approximately 2400 kcal/day, whereas the calorie-restricted group consumed approximately 1200 kcal/day. Twenty-four-hour mean glucose levels remained unchanged in the control group (6.7 +/- 0.8 mM wk 1 vs. 6.8 +/- 0.8 mM wk 2), although they dropped dramatically in the calorie-restricted group (6.7 +/- 1.0 mM wk 1 vs. 5.4 +/- 0.5 mM wk 2, P less than 0.01). Fasting plasma insulin also declined in the calorie-restricted group (265 +/- 165 pM wk 1 vs. 145 +/- 130 pM wk 2), resulting in a significant change between groups (P less than 0.02). Surprisingly, fasting plasma glucose and glucose tolerance measured by the 3-h oral glucose tolerance test did not change within or between groups. Fasting levels of beta-hydroxybutyrate rose in the calorie-restricted group (290 +/- 240 microM wk 1 vs. 780 +/- 30 microM wk 2) but not in the control group (P less than 0.01). Finally, urine ketones increased significantly (P less than 0.02) in the calorie-restricted group, whereas they remained absent in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metabolic effects of 1200-kcal diet in obese pregnant women with gestational diabetes. 222 31

The winter athlete has several potential tactics for sustaining body temperature in the face of severe cold. An increase in the intensity of physical activity may be counter-productive because of increased respiratory heat loss, increased air or water movement over the body surface, and a pumping of air or water beneath the clothing. Shivering can generate heat at a rate of 10 to 15 kJ/min, but it impairs skilled performance, while the resultant glycogen usage hastens the onset of fatigue and mental confusion. Non-shivering thermogenesis could arise in either brown adipose tissue or white fat. Brown adipose tissue generates heat by the action of free fatty acids in uncoupling mitochondrial electron transport, and by noradrenaline-induced membrane depolarisation and sodium pumping. The existence of brown adipose tissue in human adults is controversial, and although there are theoretical mechanisms of heat production in white fat, their contribution to the maintenance of body temperature is small. Acclimatisation to cold develops over the course of about 10 days, and in humans the primary change is an insulative, hypothermic type of response; this reflects the intermittent nature of most occupational and athletic exposures to cold. Nevertheless, with more sustained exposure to cold air or water, humans can apparently develop the humoral type of acclimatisation described in small mammals, with an increased output of noradrenaline and/or thyroxine. The associated mobilisation of free fatty acids suggests the possibility of using winter sport as a pleasant method of treating obesity. In men, a combination of moderate exercise and facial cooling induces a substantial fat loss over a 1- to 2-week period, with an associated ketonuria, proteinuria, and increase of body mass. Possible factors contributing to this fat loss include: (a) a small energy deficit; (b) the energy cost of synthesising new lean tissue; (c) energy loss through the storage and excretion of ketone bodies; (d) catecholamine-induced 'futile' metabolic cycles with increased resting metabolism; and (e) a specific reaction to cold dehydration. Current limitations for the clinical application of such treatment include uncertainty regarding optimal environmental conditions, concern over possible pathological reactions to cold, and suggestions of a less satisfactory fat mobilisation in female patients. Possible interactions between physical fitness and metabolic reactions to cold remain controversial.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Adaptation to exercise in the cold. 388 60

The aim of this study was to examine the long-term effects of synthetic chow diet on the metabolic pattern of diabetic syndrome in a large group of sand rats. Few animals had a fulminating reaction with markedly decreased glucose tolerance, low plasma insulin levels and death within 3-4 weeks. But the most of sand rats developed obesity and elevated plasma insulin levels. From the third month, 40% of sand rats presented a diabetic syndrome with hyperinsulinemia, hyperglycemia, markedly decreased glucose tolerance and insulin resistance. Plasma lipids were increased; the lipid and glycogen accumulation in the liver was high. So this diabetic syndrome can be compared to maturity onset diabetes. If this synthetic chow diet lasted more than 6 months, the most of animals lost considerable weight with a strong lipid depletion of fat stores. Serum immunoreactive insulin levels fall and the blood glucose rose over 500 mg/100 ml with glycosuria and ketonuria . The elevated triglyceride content of plasma and the lipid deposits in the liver were exaggerated; glycogen had disappeared. Animals developed an overtly insulin- dependent diabetes, the latter phase of the disease. The sand rat appears to us as a potentially interesting model for investigation both maturity onset and ketotic-type diabetic syndrome.
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PMID:[Appearance and metabolic development of diabetes mellitus in the sand rat, Psammomys obesus]. 623 80

It has been reported that sand rats, naturally feeding on low-caloric-value plants containing a high concentration of salt, become obese and develop hyperglycemia when fed on a standard laboratory diet. The aim of this study was to examine the long-term effects of a synthetic-chow diet on the metabolic pattern of the diabetic syndrome in a large group of sand rats. While a few animals had a fulminant reaction with markedly decreased glucose tolerance, low plasma insulin levels, and death within 3-4 wk, most sand rats developed obesity and elevated plasma insulin levels. From the third month and forward, 40% of sand rats presented with a diabetic syndrome with hyperinsulinemia, hyperglycemia, markedly decreased glucose tolerance, and insulin resistance. This diabetic syndrome can be compared with maturity-onset (type II) diabetes. When this synthetic-chow diet was given for more than 6 mo, the majority of animals lost considerable weight and showed a major depletion of fat stores. Serum immunoreactive insulin levels fell, while blood glucose rose to above 500 mg/dl with glycosuria and ketonuria. The elevated triglyceride content of plasma and the lipid deposits in the liver were greatly augmented, and no glycogen was present. Animals developed frank insulin-dependent diabetes, and diabetic animals not treated with insulin died in diabetic coma with presumed ketoacidosis. The disease was essentially confined to sand rats showing abnormal glucose tolerance, even before eating laboratory chow. This observation suggests a genetic factor. Thus, the sand rat appears to be a potentially interesting model for investigation of both maturity-onset and insulin-dependent diabetes.
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PMID:Diabetes mellitus in sand rats (Psammomys obesus). Metabolic pattern during development of the diabetic syndrome. 637 52

Insulin binding to monocytes was assessed before and after plasma insulin suppression by diazoxide in 14 obesity-related diabetic subjects. Four of the five patients with mild carbohydrate intolerance (FBS less than 150 mg%) and hyperinsulinism exhibited low monocyte insulin binding. Despite an increase in insulin binding after 7 days of diazoxide therapy, no improvement in carbohydrate tolerance could be demonstrated. Lack of improvement may have been related to persistent diazoxide effect. An additional group of 4 patients with low plasma insulin values and more severe carbohydrate intolerance (FBS greater than 150 mg%) had high monocyte insulin binding. This group, as well as a group of patients with intermediate insulin responses, tolerated diazoxide poorly and developed moderate ketonuria or severe hyperglycemia (plasma glucose greater than 350 mg%) necessitating discontinuation of the drug after 3-6 days. The studies in these patients suggest that obesity-related diabetes may be characterized early by mild elevation of plasma glucose, hyperinsulinism and impaired monocyte insulin binding. As beta cell exhaustion occurs, more severe hyperglycemia intervenes and insulin binding to monocytes increases.
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PMID:Role of insulin receptors in obesity-related diabetes. 675 56

To characterize the clinical pathologic and morphologic features of spontaneous age-related changes in pancreatic islets observed in Crl:CD (SD)BR rats, I reviewed data from rats used as controls in 10 toxicity studies from 1987 to 1992. Rats were 3.5-26 mo old at necropsy. At necropsy, rats were weighed, and serum, urine, and pancreas samples were collected. Serum was analyzed for glucose, triglyceride, and cholesterol concentrations; urine was analyzed for glucose and ketones; and samples of pancreas were stained with hematoxylin and eosin, Masson's trichrome stain, or for insulin by an immunoperoxidase method with a Masson's trichrome counterstain and examined microscopically. Male rats gained weight more rapidly than females and were visibly obese by 5 mo. Weight gain was accompanied by increased fasting triglyceride and cholesterol concentrations. Triglyceride increased more than cholesterol: from 3.5 to 17 mo of age, triglyceride concentrations increased 3.4-fold in males and 3.1-fold in females. By 14 mo of age, rats generally had fasting triglyceride concentrations > 200 mg/dl (2.2 microM). Fasting glucose concentrations generally were slightly (< 30%) greater in males than females. More males than females had glucose > 200 mg/dl (11 mM); several males had glucose > 300 mg/dl (16.5 mM). Glucosuria was not detected in any rat. Ketonuria was much more common in males than in females, but its incidence did not parallel that of obesity and hypertriglyceridemia; instead, ketonuria was most common in young males and decreased with age. Morphologic islet changes were observed in rats as young as 3.5 mo old, and their incidence increased with age.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Age-related pancreatic islet changes in Sprague-Dawley rats. 807 22


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