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

Primary fetal hepatocyte cultures derived from Zucker rats and with expected fa-gene frequencies of 0.0 and 0.75 have been established and can be used to detect early effects of the fa gene on hepatocellular metabolism. Proliferative capacity is similar in both types of culture. Changes of the growth media significantly decrease total lipogenesis in both 0.0 and 0.75 fa-gene culture grown in arginine-free DME medium. Paired incubation experiments demonstrate that total lipogenesis in 0.75 fa gene cultures is significantly less than in 0.0 fa-gene cultures under basal conditions. Stimulation of total lipogenesis by pharmacological doses of insulin and excess substrate (glucose) is significantly less in the 0.75 fa gene than in the 0.0 fa-gene cultures. These data suggest that the development of obesity in the Zucker rat cannot be attributed to elevated hepatic lipogenesis in the fetus.
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PMID:Primary cultures of fetal hepatocytes from the genetically obese Zucker rat: characterization and total lipogenesis. 699 75

Spontaneous diabetes mellitus has been observed in a female New Zealand white rabbit. By inbreeding of this individual and her offspring, 39 litters comprising 157 animals have been studied and a closed colony of diabetic rabbits established. Three groups of animals can be identified. Twenty-nine (19%) have overt diabetes characterized by fasting hyperglycemia and depressed intravenous glucose stimulated serum insulin levels. This abnormality is seen between 1 and 3 yr of life. Forty-three of the animals (27%) have developed abnormal glucose disposal with normal or slight elevations in fasting serum glucose levels. Glucose stimulated insulin levels are also significantly lower in the rabbits with abnormal glucose disposal. The remaining 85 animals (54%) exhibit no apparent abnormalities of glucose metabolism. All animals with overt diabetes pass through a stage in which glucose disposal as measured by k values is less than 1.0, a value not observed in normal animals. Fasting and arginine stimulated glucagon levels were no different in 4 diabetic animals and 7 normal colony rabbits. Insulin therapy corrected the hyperglycemia in the diabetic rabbits. Insulin was withheld in 5 diabetic rabbits and serum and urinary glucose and ketones were measured for 9 days. Despite marked increases in serum and urinary glucose, only mild ketonemia was observed. The relatively late onset of diabetic symptoms, lack of obesity, severe hyperglycemia, and depressed insulin secretion without ketoacidosis make this a model with many of the characteristics of insulin responsive diabetes as seen in nonobese human adults.
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PMID:Spontaneous diabetes mellitus in the New Zealand white rabbit: physiologic characteristics. 700 1

Glucagon secretion was studied in rats with electrolytic lesions of the bilateral ventromedial hypothalamic area (VMH-L) under various experimental conditions. The results obtained are as follows: 1. The basal plasma level of immunoreactive glucagon (IRG) was lowered in VMH-L rats 5 and 10 weeks after the operation. Plasma IRG levels after 24-hour starvation and during the arginine load were more significantly decreased in the VMH-L rats than in the control group. 2. The basal plasma level of immunoreactive insulin (IRI) showed significant positive correlations with body weight and Lee's index in these rats. The basal plasma level of IRG showed significant negative correlations with body weight, Lee's index and basal plasma IRI level. 3. In response to the arginine load, the plasma IRI level was significantly increased in VMH-L rats immediately after the operation, and the plasma IRG level was more significantly decreased in VMH-L rats 1 week after the operation than in the control group. 4. The response of plasma IRG to the arginine load was also lowered more in VMH-L rats than in rats pair-fed for 4 weeks after the operation. 5. 15 weeks after the operation, there was no significant difference in response of plasma IRI and IRG to the subcutaneous injection of epinephrine between VMH-L and control rats. These findings indicate that hypoglucagonemia in the VMH-L rats was induced by various factors, such as disorder of the autonomic nervous system, excessive insulin release, etc. The impairment of glucagon secretion may contribute to the development of obesity observed in rats with VMH-lesions.
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PMID:[Studies on glucagon secretion in obese rats with hypothalamic lesions (author's transl)]. 700 30

The effect of weight loss and caloric restriction on plasma glucose concentrations and insulin and glucagon secretion in response to oral and iv glucose and arginine infusions was examined in 8 subjects with type II diabetes mellitus of greater than 5 yr duration (long term diabetes). The findings of this study were compared to previous results in 10 subjects with similar degrees of obesity and fasting hyperglycemia but diabetes of less than 2 yr duration (recent-onset diabetes; fasting plasma glucose, 267 +/- 16.5 mg/dl in long term diabetics and 259 +/- 8.0 mg/dl in recent onset diabetics) and to a control group of 8 similarly obese but nondiabetic subjects. Both diabetic groups had impaired insulin responses on initial and final tests compared to control subjects. Response to dietary therapy was significantly poorer in the diabetics of longer duration (final fasting plasma glucose, 175 +/- 18.9 mg/dl in long term vs. 119 +/- 6.2 mg/dl in recent-onset subjects; P less than 0.01) despite a similar degree of weight loss and duration of diet therapy in the 2 groups. This difference in glucose tolerance occurred despite similar final insulin and glucagon responses in the diabetic groups. Subjects with type II diabetes of long duration appear to have a relatively greater degree of insulin resistance than subjects with more recent onset of the disease.
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PMID:Diminished effect of caloric restriction on control of hyperglycemia with increasing known duration of type II diabetes mellitus. 702 80

Responsiveness of glucagon secretion to various stimuli was examined in Zucker fatty rats. Epinephrine infusion and cold exposure increased the plasma glucagon level to the same extent in fatty and lean rats, although the plasma glucose responses to these stimuli were much higher in fatty rats than in lean rats. Glucagon secretion in response to hypoglycemia due to insulin administration was markedly blunted in fatty rats. When arginine was infused, fatty rats showed enhanced secretion of glucagon and insulin, and elevation of plasma glucose as compared with lean rats. Streptozotocin (STZ)-treatment of fatty rats decreased insulin response to arginine but had no effect on exaggerated glucagon secretion. Arginine-stimulated glucagon secretion of lean rats was exaggerated by STZ treatment. From these results, glucagon secretion of fatty rats seemed unresponsive to inhibitory effects of glucose and insulin. The ventromedial hypothalamus-lesioned obese rats showed enhanced secretion of glucagon and insulin, and elevation of plasma glucose in response to arginine as observed in fatty rats. We conclude that the abnormalities of A cells in fatty rats are presumably secondary to obesity rather than caused by the fa gene.
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PMID:Abnormal glucagon secretion in Zucker fatty rats. 726 23

A survey of fasting whole blood amino acids in 65 patients with various subtypes of retinitis pigmentosa performed. Eight X-linked recessive patients showed decreased taurine and aspartate. Nineteen autosomal recessive patients, and to lesser extent 10 autosomal dominant patients, showed reduced levels of whole blood threonine and histidine. Branched-chain amino acids and arginine were present in increased amounts in 2 patients with Laurence-Moon-Bardet-Biedl syndrome. These findings in LMBB patients are probably related in part to their obesity and emphasise that appropriate controls are required, and other factors (including age) known to affect amino acid levels must be accounted for. The biochemical implications of our findings are not yet apparent.
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PMID:Amino acids in retinitis pigmentosa. 729 29

The empty sella results from an extension of the subarachnoid space into an intrasellar position with subsequent remodeling of the sella turcica and the flattening of the pituitary gland. The sella turcica is usually enlarged causing the greatest diagnostic difficulty to distinguish it from a pituitary tumor. The most patients with this syndrome usually have normal pituitary function, while about 30% have varying degrees of hypopituitarism. The Authors describe a case report of a man with primary empty sella syndrome come to the medical observation for obesity and hyperglyccemia. The endocrine evaluation performed (TRH test, GN-RH test, T3, T4, FT3, FT4, Arginine test, metyrapone test) were normal. OGTT shows a maturity onset diabetes (glycemia = 160 mg%). This rare clinical association is not well understood. Probably this diabetes is to the interruption of the normal hypothalamo-pituitary neurovascular connection.
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PMID:[The primary empty sella syndrome. A case report study (author's transl)]. 747 Jan 79

The Trp 64 Arg mutation in the beta 3-adrenergic receptor (beta 3AR) gene was investigated in 350 Japanese subjects. This mutation was not associated with non-insulin-dependent diabetes mellitus (NIDDM). In 191 subjects without NIDDM, body mass index (BMI) was significantly higher in subjects homozygous for this mutation than in those homozygous for the normal allele (24.7 +/- 1.4 vs 22.1 +/- 0.2 kg/m2, p = 0.009). Moreover, the frequency of the mutant allele in obese subjects (BMI > 26.4) was significantly higher than that in non-obese subjects (BMI < 22) (0.37 vs 0.15, p = 0.009). The presence of this mutation was also accompanied by significantly higher fasting (p = 0.000) and 2 hrs (p = 0.018) serum insulin levels during an oral glucose tolerance test. The beta 3AR may be one of the loci contributing to obesity and hyperinsulinemia/insulin resistance in Japanese subjects.
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PMID:A mutation in the beta 3-adrenergic receptor gene is associated with obesity and hyperinsulinemia in Japanese subjects. 748 91

A recent study (1) reported variation among men in clotting factor VIIc levels is associated with a genetic polymorphism detected by the restriction enzyme Msp I. The present study determined the Msp I genotype (Arg353, Gln353 alleles) for 189 women (mean age 53) who were subjects in the Healthy Women Study, a population study of CHD risk factor change at menopause. Women with the Arg/Arg genotype (n = 147) had an 16% higher (geometric) mean FVIIc level than those with the Arg/Gln (n = 41) genotype (1.21 vs 1.04 U/ml, p < 0.01), while the one subject with the Gln/Gln genotype had an FVIIc level of 1.00 U/ml. These results are consistent with those previously found in healthy men (1). In addition, women carrying the Gln allele did not exhibit the elevation in FVIIc with menopause and use of hormone therapy found among those with the Arg allele, suggesting that genotype may modify the observed rise in factor VIIc at menopause. Possibly because of the small sample size this interaction did not reach conventional levels of statistical significance. Results of multiple linear regression analyses controlling for age, hormone use, obesity, (ln) triglyceride levels, and family history of CHD found FVIIc levels to be significantly (p < 0.001) related to genotype. Thus, genotype appears to be a major determinant of FVIIc levels among women.
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PMID:Genetic determination of coagulation factor VIIc levels among healthy middle-aged women. 749 69

Obese (ob) gene expression in abdominal subcutaneous adipocytes from lean and obese humans was examined. The full coding region of the ob gene was isolated from a human adipocyte cDNA library. Translation of the insert confirmed the reported amino acid sequence. There was no difference in the sequence of an reverse transcription PCR product of the coding region from five lean and five obese subjects. The nonsense mutation in the ob mouse which results in the conversion of arginine 105 to a stop codon was not present in human obesity. In all 10 human cDNAs, arginine 105 was encoded by CGG, consequently two nucleotide substitutions would be required to result in a stop codon. To compare the amount of ob gene expression in lean and obese individuals, radiolabed primer was used in the PCR reaction with beta-actin as a control. There was 72% more ob gene expression (P < 0.01) in eight obese subjects (body mass index, BMI = 42.8 +/- 2.7) compared to eight lean controls (BMI = 22.4 +/- 0.8). Regression analysis indicated a positive correlation between BMI and the amount of ob message (P < 0.005). There was no difference in the amount of beta-actin expression in the two groups. These results provide evidence that ob gene expression is increased in human obesity; furthermore, the mutations present in the mouse ob gene were not detected in the human mRNA population.
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PMID:Evidence against either a premature stop codon or the absence of obese gene mRNA in human obesity. 776 11


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