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

Obese mice (C57BL/6J ob/ob) and their lean controls were studied longitudinally from immediately post-weaning until 62 wk of age, at which time the experiment was terminated. The dynamic nature of the metabolic aberrations of the obese mouse syndrome was clearly demonstrated. Obese mice were hyperinsulinemic at all ages yet the concentration of glucose in plasma was elevated only at 5-20 wk and 63 wk of age, but was similar to that of lean mice at 20-60 wk of age. Triacylglycerols accumulated in the liver of obese mice between 5 and 18 wk of age to a level that was 20-fold greater than that found in the age-matched lean control. A decreased concentration of DNA/g of liver was also found in 5-18 wk-old obese mice, indicative of an enlarged hepatocyte. With the exception of 5-wk-old animals, total DNA per liver was increased in obese mice when compared to the lean control throughout the profile. Following the peak in 18-wk-old mice, the hepatic content of triacylglycerols precipitously fell so that at 45 wk of age its concentration in obese mice was similar to that of the lean control. Plasma free fatty acid levels as well as liver glycogen content were comparable in obese mice and their lean controls throughout the profile. In obese mice older than 45 wk of age, the content of triacylglycerols in plasma was significantly lower than that of the age-matched lean control while an accumulation of liver triacylglycerols was again found in obese mice. Myocardial triacylglycerols were elevated in obese mice when compared to the lean control at all ages. The longitudinal metabolic profile of the obese mouse developed in the present study clearly demonstrates the dynamic nature of the deviations in carbohydrate and lipid metabolism in this animal model of human obesity and insulin resistance.
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PMID:Age-related changes in lipid and carbohydrate metabolism of the genetically obese mouse. 633 47

Variations in DNA sequences flanking the insulin gene were studied in relation to noninsulin-dependent diabetes mellitus (NIDDM) in 87 unrelated Pima Indians at least 35 yr of age. DNA was isolated from nuclei of peripheral blood leukocytes and digested with restriction endonucleases. Less variation in this region was found in Pima Indians than in other racial groups previously studied. Only two classes of alleles (classes 1 and 3) were found, and there was virtually no variation within classes. At least one class 3 allele was found in 47% of the 38 nondiabetic subjects and in 37% of the 49 with NIDDM (odds ratio = 0.65, P = 0.4, 95% confidence interval for the odds ratio = 0.25 to 1.67). Homozygosity for class 3 alleles, however, was found only in diabetics. There were no differences according to genotype in obesity, fasting or postload glucose or insulin concentrations, or in the relationships between insulin and glucose concentrations. 61% (11/18) of the diabetics with a class 3 allele were receiving drug treatment for diabetes compared with only 26% (8/31) of diabetics without a class 3 allele (P = 0.03). The insulin gene polymorphism probably plays no important role in the genesis of NIDDM in Pima Indians, nor does it influence the glucose or insulin concentrations or their relationship to each other, but the class 3 allele, especially when homozygous in this population, may influence the severity of the disease as indicated by need for drug treatment.
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PMID:Polymorphism in the 5' flanking region of the human insulin gene. Relationships with noninsulin-dependent diabetes mellitus, glucose and insulin concentrations, and diabetes treatment in the Pima Indians. 639 41

Changes of the pyruvate dehydrogenase complex in liver and epididymal fat pad were examined longitudinally in obese mice (C57BL/6J-ob/ob) and their lean controls as a function of age. Total pyruvate dehydrogenase in liver was expressed on several reference bases because of differences in hepatic cellularity and protein content between obese mice and their age-matched lean controls. When total hepatic pyruvate dehydrogenase was expressed on a protein basis, the enzyme activity was elevated in obese mice older than 28 weeks in age when compared to lean controls of a similar age. However, when expressed on a DNA basis, total pyruvate dehydrogenase activity in livers of obese mice up to 10 weeks in age was increased when compared to the age-matched lean control. The proportion of hepatic pyruvate dehydrogenase in the active form was also augmented significantly in obese mice from 5 to 28 weeks of age. In 18-week-old obese mice, the proportion of total pyruvate dehydrogenase in the active form of adipose tissue was significantly higher than that of the lean controls. When expressed on a DNA basis, total pyruvate dehydrogenase in the fat pad was also increased in obese mice up to 10 weeks in age when compared to age-matched controls. Total pyruvate dehydrogenase activity in the epididymal fat pad was higher in obese mice than the lean controls in animals as old as 32 weeks in age when the enzyme activity was expressed per 100 g body weight. The increase in the active form and total activity of pyruvate dehydrogenase in both liver and epididymal fat pad during the dynamic early phase of obesity would augment the capacity for acetyl-coenzyme A formation necessary in the support of an accelerated lipogenesis and fat deposition.
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PMID:Age-related changes in liver and adipose tissue pyruvate dehydrogenase of genetically obese mice. 671 96

In order to evaluate the long-term effects of intestinal bypass surgery in an animal model of early onset hypercellular-hypertrophic obesity, adult female obese and lean Zucker rats were given jejunoileal bypass surgery or sham operations. At sacrifice ten months post-surgery, body weights of obese bypass rats were nearly reduced to lean bypass levels. This reduction in body weight was not accompanied by normalization of body composition or of the hyperinsulinemia and hypertriglyceridemia characteristic of this obese syndrome. Obese bypass rats maintained 44 percent of their weight as lipid compared to 12 percent in lean bypass rats and 15 percent in sham-operated lean rats. In addition, obese bypass rats maintained elevated adipose tissue lipoprotein lipase activity and increased fat cell size and were hyperinsulinemic and hypertriglyceridemic. Furthermore, obese bypass rats had reduced carcass protein and reduced weight and DNA and/or protein contents in heart, liver, muscle and kidney. Therefore, although bypass surgery resulted in significant weight loss, it did not normalize the obese syndrome and may result in serious reductions in the weight and cellularity of vital organs.
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PMID:Zucker fafa rats maintain their obese body composition ten months after jejunoileal bypass surgery. 676 Dec 86

Two cases of insulin resistance are described, and recent developments in the pathogenesis and treatment of insulin resistance are reviewed. Both immune and nonimmune types of insulin resistance have been described. Immune resistance is related to the presence of circulating antibodies directed against exogenous insulin or the insulin receptor sites. Nonimmune resistance is associated with obesity, ketoacidosis, infection, or endocrinopathies. Treatment of insulin-resistant diabetics can include proper diet and weight control; use of insulin in large quantities; selection of less antigenic forms of insulin, such as pork, fish, or sulfated insulin; oral hypoglycemics such as tolbutamide; and immunosuppressive therapy with corticosteroids. The production of human insulin by recombinant DNA technology promises benefits to patients with high levels of antibodies directed against insulin from animal sources. True insulin resistance is a rare phenomenon, which must be documented adequately before vigorous treatment is considered.
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PMID:Insulin resistance: definition and treatment. 677 14

Golden hamsters fed a high-fat diet do not overeat, but they become obese because of decreases in energy expenditure. This decrease in actual energy expenditure is accompanied by increases in thermogenic capacity and brown adipose tissue mass, protein content, and DNA content. Three experiments examined this phenomenon in more detail. Experiment 1 demonstrated that this form of dietary obesity is largely reversible simply by returning the animals to a high-carbohydrate chow diet. However, the obesity which develops solely because of decreased energy expenditure is reversed primarily by decreased energy intake. In this respect fat-fed hamsters resemble tube-fed rats. Experiment 2 revealed that the effects of high-fat diet are at least as robust in female hamsters as in males. Experiment 3 examined the interactions between diet and photoperiod. Short days (10 hr light per 24 hr) had almost no effect on male hamsters fed Purina chow. However, nearly all of the effects of the high-fat diet (i.e., increases in body weight gain, feed efficiency, carcass energy content, percent ingested energy stored in the carcass, carcass lipid content, brown adipose tissue protein, and brown adipose tissue DNA) were exaggerated in hamsters housed in short days. High-fat-diet-induced increases in metabolic efficiency and thermogenic capacity may be of value in readying hamsters for winter. Furthermore, as winter approaches, decreasing day length might synergize with changes in diet quality to promote these beneficial changes in energy metabolism. Finally, fat-fed hamsters could be a useful animal model of some kinds of human obesity.
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PMID:Dietary obesity in golden hamsters: reversibility and effects of sex and photoperiod. 683 36

When male golden hamsters were switched from a diet of Purina rodent chow to a calorically-dense high-fat diet or were given ad lib access to a 32% sucrose solution in addition to chow, they adjusted their food intakes rapidly (within 24 hr) and did not overeat. Nevertheless, the fat-fed hamsters tripled their rate of weight gain and nearly doubled their carcass fat content after one month on the diet. Resting oxygen consumption (animals awake but quite) was significantly lower in fat-fed animals than in chow-fed controls. Sucrose feeding had no effect on food intake, body weight gain, carcass composition or oxygen consumption. Thus, whereas rats exhibit dietary obesity in spite of increases in energy expenditure (diet-induced thermogenesis), fat-fed hamsters seem to become obese because of decreases in energy expenditure. However, although actual energy expenditure is reduced, fat-fed hamsters exhibit an enhanced thermogenic capacity. Interscapular brown adipose tissue mass, protein content, and DNA content as well as norepinephrine-stimulated oxygen consumption were all significantly elevated in fat-fed hamsters. The significance of these concurrent diet-induced decreases in energy expenditure and increases in thermogenic capacity is not clear, but they could be of some value in preparing the hamster for winter.
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PMID:Obesity without overeating in golden hamsters. 689 Oct 78

Weanling rats fed a palatable "cafeteria" diet consumed 40-70% more energy than stock fed controls but also showed a marked (80%) increase in energy expenditure (diet-induced thermogenesis) so that body weight and body energy gain were almost identical in both groups. Animals previously fed the cafeteria diet for 30 days after weaning exhibited lower weight gains when re-exposed to the cafeteria diet at 90 days of age than either naive rats or rats which had been fed the cafeteria diet continuously from weaning. Rats which had been undernourished for 30 days form weaning and allowed to recover for 30 days showed similar responses to the cafeteria diet as normal animals. Hypertrophy of brown adipose tissue (BAT) was seen in all cafeteria fed rats but hyperplasia (increased DNA content) was observed only in rats which had been overfed in early life. These results suggest that overfeeding young, weanling rats can result in a lower fat content, a greater thermogenic capacity and resistance to obesity later in life and may be due to a permanent increase in BAT cell number.
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PMID:Effects of early overnutrition and undernutrition in rats on the metabolic responses to overnutrition in later life. 695 34

The New Zealand Obese (NZO) mouse was studied as a potential model for autoimmune diabetes. NZO mice develop obesity, glucose intolerance, and insulin resistance, and have low-titer IgM antibodies to the insulin receptor. It is shown that they have circulating antibodies to both native DNA and denatured, single-stranded DNA. The antibody levels are higher in females, and, up to 6 mo of age, are comparable to those found in the related NZB X NZW F1 (NZB/W) mouse, a model for systemic lupus erythematosus. After 6 mo of age the antibody levels in NZO mice fall toward normal, in contrast to the persistently elevated levels in NZB/W mice. NZB/W mice are known to succumb to immune complex-mediated proliferative glomerulonephritis before 1 yr of age, whereas NZO mice survive. NZO kidneys exhibit light microscopic features of both diabetic and lupus nephropathies: glomerular proliferation, mesangial deposits, mild basement membrane thickening, glomerulosclerosis, eosinophilic nodules in some glomeruli, occasional hyalinization of the glomerular arterioles, and healing arteriolar inflammation. These changes are associated with glomerular deposition of immunoglobulin, especially IgM, in a granular pattern on fluorescent staining. The NZO mouse, therefore, has evidence of a generalized immune disorder and provides a model for studying the relationship between autoimmunity, obesity, and diabetes.
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PMID:Diabetes is associated with autoimmunity in the New Zealand obese (NZO) mouse. 700 65

The chicken MHC (B complex) initially described by Briles as controlling blood antigens, is now known to be composed of at least three regions, L, F and G. Two of these, F and G, were described on the basis of recombinants found in a study of over 10,000 chickens. On the basis of biochemical, tissue distribution and functional analyses, F corresponds to the murine H-2 K/D regions. The G region is unique to the chicken since the antigenic product is expressed only on erythrocytes and their progenitors. L was identified by serological studies and corresponds to the H-2 I region; the L antigen is expressed predominantly on B lymphocytes, monocytes and 10% of T lymphocytes, and differences in the L region result in variations in immune responsiveness. A number of functional similarities exist between the chicken MHC and that of other species such as regulation of graft rejection, graft-versus-host reaction (GVHR) and mixed lymphocyte reactions (MLR), mitogenic and immune responsiveness and resistance to RNA and DNA virus infection. The chicken MHC also controls the severity of autoimmune disease, as exemplified by the spontaneous thyroiditis of Obese strain (OS) chickens. It differs from mammalian MHC's by having of lower crossing-over frequency and no apparent gene duplication.
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PMID:Chicken major histocompatibility complex and disease. 704 23


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