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

A recent development in the treatment of obesity is the widespread use of very-low-calorie diets. This study assessed the response to refeeding (RF) after semistarvation (SS) in a rat model. Male Sprague-Dawley rats (440 g) were semistarved for 21 d, receiving a nutritionally complete defined formula diet at 23% of calories of control (C) rats fed ad libitum, and subsequently refed over 21 d (SS----RF). Organ weight, contents of protein and DNA, and the protein-DNA ratio were determined for the liver, pancreas, small intestine, and heart. Compared with C animals, SS----RF animals showed variable repletion of tissue protein but not of tissue DNA. The higher protein-DNA ratio shown in these organ systems suggests a cellular hypertrophic adaptive response to refeeding. A persistent reduced number of cells in ratio to protein concentration is evident despite refeeding over 21 d. Very-low-calorie diets as well as refeeding influence nitrogen economy of selected organ systems.
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PMID:Gastrointestinal and cardiac response to refeeding after low-calorie semistarvation. 281 99

We describe a 3-year-old boy and his 2 maternal uncles with moderate to severe mental retardation, short stature, mild obesity, hypogonadism, a low total finger ridge count, and a distinctive face characterized by bitemporal narrowness, almond-shaped palperbral fissures, depressed nasal bridge, anteverted nares, short and inverted-V-shaped upper lip, and macrostomia. Two other males in this family who had similar facial anomalies and developmental delay died in early infancy and midchildhood. This apparently new disorder is reminiscent of, but distinct from, the Prader-Willi syndrome, and is likely inherited as an X-linked recessive trait. Preliminary studies with DNA probes are consistent with an X-linked locus and permit exclusion of distal Xp and Xq regions as the site of this mutation.
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PMID:Mental retardation, distinct facial changes, short stature, obesity, and hypogonadism: a new X-linked mental retardation syndrome. 323 63

We have previously shown that normal chicken serum (NCS) is able to interfere with the IL 2 promoted incorporation of DNA precursors into T lymphoblasts and that serum derived from autoimmunity prone Obese strain (OS) chickens is deficient in this respect. This "defect in non-specific suppression" has been speculated to be one of the causes for T cell hyperreactivity in the OS. In this study we present several lines of evidence that the suppressive effect of normal chicken serum (NCS) on 5-(125Iodo)-2-deoxyuridine (125IUdR) uptake into chicken T blasts is a competition artefact due to cold thymidine (TdR) present in NCS. Inhibition of 125IUdR required the continuous presence of NCS and suppression of 3H-TdR incorporation could be competed for by increasing the dose of the radiolabel. Molecular sieve chromatography followed by reversed phase high performance liquid chromotagraphy revealed the "inhibitory" activity to co-elute with TdR. Moreover, NCS did not suppress protein synthesis by chicken T cells growing with IL 2 and did not affect oxidative metabolism, cell viability, expression of IL 2 receptors, or percentages of cells in the S phase of the cell cycle. In accordance with these data, OS-sera suprisingly contain less TdR than those from normal controls. Experiments involving crosses of the OS with the normal inbred CB strain, revealed that the subnormal serum TdR level of the OS is an autosomally dominant trait which, however, segregates from T cell hyperreactivity. These findings falsify our previous hypothesis that a defect in specific IL 2 antagonists might be involved in T cell hyperfunction of the OS and indicate that NCS is devoid of factors which neutralize IL 2 function.
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PMID:Decreased level of thymidine in the serum of obese strain (OS) chickens with spontaneous autoimmune thyroiditis. 326 15

Fetuses from linebred lean (L) and linebred obese (O) and reciprocal crossmatings were examined at 110 d of gestation for line, maternal and heterotic effects. There was no significant heterotic effect for any trait measured. A significant maternal effect was observed for adipose tissue lipoprotein lipase (LPL) activity and for serum triglycerides. The enzyme activity and triglycerides concentration were higher in fetuses from O dams than in fetuses from L dams. In a lipid clearance test, no maternal effect was observed for changes in serum concentrations of triglycerides and free fatty acids or in optical density (associated with the disappearance of injected Liposyn). Linebred O fetuses exhibited higher LPL activity in both the biceps femoris muscle and sc adipose tissue compared with linebred L fetuses. The LPL activity of the adipose tissue was higher than that of the skeletal muscle. The percentage of dry matter, percentage of triglycerides and protein/DNA were higher in the muscle of linebred O fetuses than in that of linebred L fetuses. Based on tissue LPL activity and on muscle compositional traits, linebred O fetuses were more mature at 110 d of gestation than were the linebred L fetuses. Maternal obesity had little detectable influence on fetal development of the pig when measured at 110 d of gestation.
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PMID:Influence of maternal obesity on fetal development in pigs. 336 13

Obese Zucker rats were dosed orally for one week with fenofibrate (100 mg/kg). Liver weights of treated rats as expressed as percent of body weight were slightly increased, while protein, DNA and lipid contents were unaffected per g of liver or increased when expressed in whole liver. Compared with the control animals, activities of fatty acid oxidase, of the peroxisomal fatty acid-oxidizing system and of catalase were markedly increased by fenofibrate both per g of liver and per total liver, while urate oxidase activity was unchanged when expressed per g of liver. The activity of monoamine oxidase and that of cytochrome c oxidase used as marker enzymes for mitochondria were increased only when expressed per total liver. However, fenofibrate treatment induced a pronounced increase in the activities of mitochondrial palmitoyl-CoA dehydrogenase and carnitine acyltransferases, particularly carnitine acetyltransferase. Fenofibrate also caused a significant increase of carnitine content in liver and hepatic mitochondria. The greatest observed increases were in free carnitine and in the rate of carnitine-dependent oleate oxidation, which might be favoured in vivo by a lesser sensitivity of CPT-I to a malonyl-CoA inhibitory effect. The present results suggest that fenofibrate treatment induces increased hepatic mitochondrial beta-oxidation in obese Zucker rats.
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PMID:Effects of fenofibrate treatment on fatty acid oxidation in liver mitochondria of obese Zucker rats. 366 37

Maturity-onset obesity and elevated circulating insulin levels are characteristic of some, but not all, mice bearing the viable yellow mutation (Avy) at the agouti locus. The expression of the Avy/a genotype in individual mice, which become obese and which remain lean is determined during prenatal development by as yet unidentified conditions in the dam's reproductive tract. One Avy/a phenotype is identified by a mottled yellow coat and characterized by adult obesity, elevated circulating insulin levels, and impaired glucose tolerance. These mice are notably more susceptible to hyperplasia and neoplasia. The alternative Avy/ a phenotype has a pseudoagouti coat, remains lean, is normoinsulinemic and normoglycemic, and in numerous other characteristics resembles congeneic lean black (a/a) littermates. Obese mottled yellow and lean pseudoagouti Avy/a mice differ in capacity to support the growth of ascites cells, in the growth response to castration, and in hepatic glutathione S-transferase activity, erythrocyte fragility, immune function, and susceptibility to Plasmodium yoelii pathogenesis. Our working hypothesis is that the constellation of characteristics, except coat color pattern, which differentiate the obese yellow mice from their lean littermates, is largely a consequence of the elevated circulating insulin levels that induce increased lipogenesis and decreased lipolysis, increased DNA and protein synthesis, increased mitosis in sensitive tissues, and increased proliferation of transformed cells.
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PMID:Prenatal determination of obesity, tumor susceptibility, and coat color pattern in viable yellow (Avy/a) mice. The yellow mouse syndrome. 373 4

The potential of plasma from obese and non-obese subjects to stimulate the formation of new adipocytes was studied by assays in rat adipose precursor cells in primary culture. Adipogenic activity was followed in terms of rate of lipid filling, analysed by determination of triglyceride contents per unit protein, stimulation of multiplication, measured as rate of incorporation of labelled thymidine into DNA, and stimulation of differentiation, followed as an increase in glycerophosphate dehydrogenase activity. Plasma from obese subjects contained an excess of activity stimulating lipid filling, closely associated to the recent body weight histories with increased activity with a recent increase of body weight and vice versa. There was also a strong association with plasma concentration of triglyceride. The importance of the latter was demonstrated by acute feeding experiments with triglyceride, as well as by addition of isolated very-low-density lipoprotein and chylomicron fractions which caused increases of lipid filling activity closely in parallel to triglyceride contents of the culture medium. Specific stimulatory properties of plasma from weight-increasing obese subjects on adipose precursor cell multiplication and differentiation were not found. It was suggested that human obesity with an increased number of adipocytes is not characterized by elevated circulating specific stimulatory factors of new fat cell formation. Such factors are present in excess in both non-obese and obese subjects. It was hypothesized that the elevated lipid filling capacity in obese subjects might modify local inhibitory factors of adipocyte formation.
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PMID:Adipogenic activity in human plasma. Effects of feeding state and obesity. 377 Oct 91

Brown adipose tissue (BAT) thermogenesis is important in the adaptation of body energy expenditure to cold exposure, fasting, and overfeeding and in the pathogenesis of obesity. Thyroid hormones are required for the normal functioning of BAT. The mechanism of their effect on BAT, however, has not yet been elucidated. Since most thyroid hormone effects are mediated via the binding of T3 to nuclear receptors (NT3R) the present studies were performed to investigate whether BAT contained NT3R and whether these NT3R were affected by cold exposure, fasting, overfeeding, or hypo- or hyperthyroidism. Rat BAT was found to contain NT3R with a maximum binding capacity (MBC) of 0.28 ng T3/mg DNA and a dissociation constant (Kd) of 3.2 X 10(-10) M. These parameters were unaffected by any of the experimental conditions studied. A major alteration of BAT NT3R MBC or Kd is thus not a causal factor in the changes in BAT thermogenesis induced by the above experimental conditions. In contrast, 3-wk overfeeding increased (+48%) and fasting decreased (-29%) the MBC of hepatic NT3R. Overfeeding increased serum T3 (+110%), while fasting decreased it (-37%).
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PMID:Brown fat nuclear triiodothyronine receptors in rats. 377 60

The growth pattern of visceral organs was investigated in monosodium L-glutamate (MSG)-treated obese mice with hypothalamic lesions. Male Jcl-ICR strain mice were subcutaneously injected with MSG, 2 mg/g of body weight daily, for five days after birth. The MSG-treated mice became obese after 4 weeks of age. According to patterns of weight gain compared with those in the control mice, the visceral organs in the MSG-treated mice were classified into three groups as follows: The first group of organs (heart, lungs, spleen, pancreas, kidneys, testes, brain and submandibular glands) remained absolutely lower in weight throughout their growth. The second group of organs (liver and stomach) was low in weight until 12 weeks of age, but became identical to that of the control mice after 16 weeks of age. The third group of organs (epididymal fat, small intestine and colon) showed lower weight until 4 weeks of age and were significantly heavier than those in the control mice after 8 weeks of age. The heart in the first group of organs apparently had hypertrophic muscle cells after 8 weeks of age and became significantly hypoplastic due to decreased cell production as was revealed by the continuous suppression of mitotic activity and DNA synthesis by [3H]thymidine autoradiography. The liver in the second group of organs became significantly hypoplastic due to decreased cell production and showed the same weight with the control mice due to the development of fatty liver. The small intestine in the third group of organs became hypoplastic due to decreased cell production in the crypts until 4 weeks of age, and became hypertrophic and hyperplastic by the acceleration of cell production in the crypts from 4 to 8 weeks of age. From these findings, in the MSG-treated mice with specific growth patterns of visceral organs, it is suggested that low energy expenditure results in a relatively excessive energy supply and leads to obesity, because most of the important organs with major physiological functions became hypoplastic. Moreover, it seems that hypertrophy and hyperplasia of the intestine suggest a possible acceleration of the absorptive function.
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PMID:Morphological and cell proliferative study on the growth of visceral organs in monosodium L-glutamate-treated obese mice. 380 54

Lipoprotein lipase is a key enzyme of lipid metabolism that acts to hydrolyze triglycerides, providing free fatty acids for cells and affecting the maturation of circulating lipoproteins. It has been proposed that the enzyme plays a role in the development of obesity and atherosclerosis. The human enzyme has been difficult to purify and its protein sequence was heretofore undetermined. A complementary DNA for human lipoprotein lipase that codes for a mature protein of 448 amino acids has now been cloned and sequenced. Analysis of the sequence indicates that human lipoprotein lipase, hepatic lipase, and pancreatic lipase are members of a gene family. Two distinct species of lipoprotein lipase messenger RNA that arise from alternative sites of 3'-terminal polyadenylation were detected in several different tissues.
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PMID:Human lipoprotein lipase complementary DNA sequence. 382 7


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