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

Mutation diabetes in the mouse occurs in the C57BL/Ks strain. All homozygous animals (db/db) develop obesity, elevated blood sugar levels and increased or normal blood insulin concentration. The defects in cellular immunity in db/db mice and their littermate controls were examined both in vivo and in vitro. Significant suppression of delayed footpad swelling and first and second set skin allograft rejection time were observed. In addition, DNA synthesis in spleen cells after nonspecific mitogen stimulation was markedly inhibited. Diabetic animals with a mean blood sugar of 512 +/- 101 mg/100 ml did not respond to exogenous insulin therapy by lowering their blood sugar levels or reversing the defect in DNA synthesis. Adding insulin to spleen cell culture in vitro had no demonstrable effect on their response to mitogens. Thus, mutation diabetic mice with their known defect in the peripheral utilization of insulin have markedly suppressed cell-mediated immune mechanisms.
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PMID:Impairment of cell-mediated immunity in mutation diabetic mice (db/db). 34 1

Thymidine kinase activity and the pattern of DNA accretion in the genetically obese Zucker rat (fafa) were shown to develop in a manner fundamentally different from that of the lean rat. In normal lean Zucker rats, fat cell size and number, thymidine kinase activity, total DNA, and DNA in lipid-filled and nonlipid-filled tissue changed as previously reported for the normally growing lean Sprague-Dawley rat. In the epididymal depot of the developing obese rat, the progressive obesity is characterized by marked early enlargement of fat cell size, elevated thymidine kinase activity until 273 days of age, increased rate of total tissue DNA accretion until 182 days of age, and fat cell hyperplasia that becomes manifest after an apparent "peak" cell size is reached at 98 days of age.
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PMID:Developmental changes in thymidine kinase, DNA, and fat cellularity in Zucker rats. 44 70

Three techniques for overfeeding rat pups were used from birth to 24 days of age to assess their effect on growth and development in an obesity susceptible (OM) and an obesity resistant (S 5B/P1) strain of rat. These included: (1) Feeding a semi-purified high fat rather than low fat diet to the dams (alters the energy content of milk); (2) Raising pups in litters of 3 rather than 6; and (3) Force feeding of milk in lieu of any force feeding. In OM rats there was no difference in lean body mass (excludes heart, liver and kidney) (LBM) gastrocnemius muscle weights, cell number and protein content of muscle. Body weights and gastrocnemius muscle triglycerides were significantly higher in OM rats fed the high fat diet than in those fed the low fat diet. S 5B/P1 (S) rats treated in the same manner as OM, showed no significant differences in body weight, LBM, gastrocnemius muscle weight or content of DNA, protein or triglycerides. Protein and DNA for 100 g fresh gastrocnemius muscle were similar for the two strains even though the muscle was 1 1/2 times heavier in OM than in S rats. Muscle triglycerides were higher in OM than in S rats.
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PMID:Growth and development of gastrocnemius muscle in S 5B/PL and Osborne-Mendel rats overfed during nursing. 56 15

The significance of fat accumulation during physiological development of layers was studied using White Leghorn X Australorp pullets from 12 weeks of age. 2. Liver fat, carcass fat, liver weight and body weight increased markedly at the onset of sexual maturity. 3. Within the liver, the protein to DNA ratio did not alter significantly during development; glycogen was not consistently depleted by egg production. 4. Liver fat content was significantly correlated with carcass fat, liver weight and DNA concentration, and plasma total lipid and cholesterol, independent of stage of development; with body weight, liver protein, moisture, and protein to DNA ratio, excluding the period prior to commencement of sexual maturation; and with plasma phospholipid during lay. 5. Obesity was a feature of faster growing fowls which matured earlier, consumed more, utilised food less efficiently for egg production and produced fewer saleable eggs.
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PMID:Biochemical, physiological and production indices related to fat metabolism in the laying fowl at various stages of physiological development. 89 May 17

Skeletal muscle growth in two genetic lines of pigs that differed in total muscle content was studied at live weights of 23, 45, 68, 91, 104, 118 kg. Total physically separable muscle and cross-sectional area of the longissimus dorsi muscle were greater in the muscular than in the obese genetic lines. Above 45 kg, animals in the muscular genetic line had less total separable fat than animals in the obese line, but the two lines did not differ in total physically separable fat at 23 and 45 kg live weight. Hence, these two genetic lines may differ in weight at which maturity is reached as much as in inherent propensity for obesity. Longissimus muscle form the muscular line had more water, less protein, and less lipid than longissimus from the obese line. DNA and RNA concentration, total DNA and RNA content, and RNA/DNA ratio of the pituitary and liver did not differ between the two genetic lines. Above 68 kg, longissimus from the muscular line had higher DNA and RNA concentrations than longissimus from the obese line; this difference did not exist between 23 and 68 kg. RNA/DNA ratio of the longissimus muscle was greater and protein-to-DNA and protein-to-RNA ratios in longissimus were lower in the muscular than in the obese line. Total DNA content of physically separable muscle increased 2.0 (obese) to 2.7 (muscular)-fold between 23 and 118 kg; hence, number of muscle nuclei increases during growth. Total DNA content of physically separable muscle was greater in the muscular than in the obese line and was the measurement most highly related to total muscle content.
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PMID:Muscle growth in two genetically different lines of swine. 97 69

Previous studies showed that atrophy of brown adipose tissue (BAT) of capsaicin-desensitized rats occurs rapidly and persists for up to 28 days. The rats do not, however, become any more obese than control rats, despite the frequent association of atrophied BAT with obesity. The objective of the present study was to assess longer-term effects of capsaicin desensitization on BAT and on energy balance. Rats were studied at 2.5, 3.5, and 8 mo after treatment. Major effects at 8 mo, mostly seen to a lesser extent at 3.5 mo but not at 2.5 mo, were a marked reduction in body weight that was largely attributable to a reduction in body fat but also to some stunting of growth and an atrophy or lack of growth of BAT (reduced weight and content of protein, DNA, cytochrome oxidase, and uncoupling protein). Resting metabolic rates and food intake at 8 mo were reduced in proportion to the smaller body size. We suggest that the lack of trophic influence of sensory neuropeptides on BAT proposed previously may extend to other organs, including white adipose tissue, and contribute to the reduced adiposity and the smaller body size of capsaicin-desensitized rats.
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PMID:Long-term decrease in body fat and in brown adipose tissue in capsaicin-desensitized rats. 131 15

The concordance of clinical and molecular genetic diagnoses of heterozygous familial hypercholesterolemia (FH) was studied in 65 subjects (10 propositi and 55 first-degree relatives) from 10 families with FH. Nine propositi were carriers of the FH-Helsinki deletion of the low density lipoprotein (LDL) receptor gene, prevalent in the Finnish population, while a new deletion, extending from intron 14 to intron 15 of the LDL receptor gene, was identified in one family. Serum LDL cholesterol levels used in the clinical diagnosis (less than 5.0 mmol/l, not FH; 5.0-5.9 mmol/l, possible FH; greater than or equal to 6.0 mmol/l, FH; limits are 1 mmol/l lower for those less than 18 years) were derived from an authoritative recommendation. Tendon xanthomas constituted an additional criterion. With the DNA analysis as the reference, 55 (85%) subjects could be correctly classified clinically as FH patients or subjects without FH. The remaining 10 subjects were misclassified or were in the "possible FH" category. When the age- and sex-specific 95th percentile LDL cholesterol levels were used instead of the rigid values for both adults and children, the percentage of correct diagnoses rose to 95%. Common genetic polymorphisms of apolipoproteins E and B did not markedly affect LDL cholesterol levels in FH patients, whereas increasing age and obesity were associated with elevated LDL levels. In conclusion, DNA analysis is a valuable adjunct to the diagnosis of FH that is applicable to families with a known mutation of the LDL receptor gene. If DNA methods are not available, age- and sex-specific LDL levels should be used as an aid in the clinical diagnosis of FH.
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PMID:Diagnosis of heterozygous familial hypercholesterolemia. DNA analysis complements clinical examination and analysis of serum lipid levels. 131 70

Hypertriglyceridemia is frequently associated with obesity. In the general Caucasian population, an association of the uncommon S2 allele of a DNA polymorphism of the apolipoprotein (apo) A-I/C-III/A-IV gene cluster with hypertriglyceridemia has been reported. To assess the risk of hypertriglyceridemia associated with the S2 allele in obesity, lipid status and apo A-I/C-III/A-IV genotypes were studied in 90 unrelated Caucasian obese subjects. Age, body mass index, percentage body fat and waist-hip ratio were comparable between genotypes. The frequency of S1/S2 genotype was 35% in the hypertriglyceridemic group versus 11.4% in the normotriglyceridemic group (P < 0.05). The odds ratio of hypertriglyceridemia was 3.7 for obese subjects with the S2 allele and 26.7% of hypertriglyceridemias could be attributed to the S2 allele. Women with the S1/S2 genotype had also significantly higher VLDL- and LDL-cholesterol concentrations. These results suggest that the S2 allele modulates the effects of obesity on lipoproteins and increases the risk of hypertriglyceridemia when obese.
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PMID:Association of a DNA polymorphism of the apolipoprotein A-I/C-III/A-IV gene cluster with hypertriglyceridemia in obese people. 133 44

A DNA mapping panel derived from an interspecific backcross was used to position the mouse insulin-2 locus (Ins-2) on Chromosome 7, near H19 (0/114 recombinants) and Th (1/114 recombinants). Ins-2 is part of a human-mouse conserved linkage group that includes Th, H19, and Igf-2. Analysis of segregation in the F2 generation from the cross C57BL/6J-tub/tub x CAST/Ei demonstrated that Ins-2 and the obesity mutant tubby (tub) are distinct loci, thus eliminating Ins-2 as a candidate gene for tub. These results also refine the estimated genetic distance between tub and Hbb to 2.4 +/- 1.4 cM. The predicted location for a human homolog of tubby is HSA 11p15.
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PMID:Localization of insulin-2 (Ins-2) and the obesity mutant tubby (tub) to distinct regions of mouse chromosome 7. 135 94

The significance of variation within the genes coding for three glucose transporter proteins in the aetiology of non-insulin dependent diabetes mellitus was assessed by analysing restriction fragment length polymorphisms in an English Caucasian population. Two polymorphisms at the HepG2/erythrocyte glucose transporter (GLUT1) locus, four at the liver/pancreatic glucose transporter (GLUT2) locus and one at the muscle/adipocyte glucose transporter (GLUT4) were analysed in a sample of diabetic and non-diabetic subjects. No significant differences in the allelic, genotypic or haplotypic frequencies of the polymorphisms at these three loci were observed between the diabetic or non-diabetic populations. No significant linkage disequilibrium was observed between the two GLUT1 polymorphic sites, whereas the four polymorphic sites at the GLUT2 locus, one of which appears to be due to a 100-200 base pair DNA insertion/deletion, were found to be in significant linkage disequilibrium. In order to study the possible role of glucose transporter gene variants contributing to the development of obesity, the body mass indexes were compared in the different genotypic groups of diabetic and non-diabetic subjects. No differences in body mass index between genotype groups were found at the p < 0.005 level of significance.
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PMID:Analysis of three glucose transporter genes in a Caucasian population: no associations with non-insulin-dependent diabetes and obesity. 136 30


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