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

This paper summarizes data obtained in our laboratory on the demonstration of receptors for IgG-Fc (FcR) and complement (CR) on mononuclear cells of the fowl. A clearcut distinction of these two structures on spleen cells was achieved in rosette assays using SRBC coated with rabbit IgG as indicator cells which bind avian complement, but are not bound by the FcR. The tissue distribution and localization of FcR and CR positive cells was studied in mixed hemadsorption assays on sections of both central (bursa, thymus) and peripheral (spleen) lymphoid organs from normal chickens, as well as lymphocytic infiltrated thyroid glands from animals of the Obese strain (OS) afflicted with spontaneous autoimmune thyroiditis. The possible significance of both receptors in the pathogenesis of this autoimmune process is discussed.
Mol Immunol 1982 Oct
PMID:IgG-Fc and C3 receptors in the chicken: distribution, tissue localization and functional significance. 689 42

Age is known to be associated with the development of glucose intolerance. In this review an effort has been made to differentiate between the effects of age per se on glucose tolerance, as distinguished from those of such age-related variables as obesity, diet, development of frank diabetes, etc. At the same time, an attempt was made to evaluate the evidence implicating abnormalities of insulin secretion and/or insulin action in the development of glucose intolerance with age. It is concluded that the questions being asked are far from simple, and that available data do not provide unequivocal answers.
Mol Cell Biochem 1980 May 28
PMID:Effects of age on various aspects of glucose and insulin metabolism. 699 16

Adipocytes from 26-week-old Zucker rats (greater than 600 g) and controls of the same strain and age (greater than 400 g) served as models of insulin resistance and obesity. Adipocytes from fatty rats demonstrated insulin resistance of glucose metabolism and resistance to the antilipolytic effect of insulin which was not improved by fasting. Adipocytes from fatty rats were also resistant to the lipolytic action of norepinephrine. Control rats displayed insulin resistance of glucose metabolism and resistance to the antilipolytic effect of insulin. However, fasting for 6.5 days restored the antilipolytic action of insulin without affecting the insulin sensitivity of glucose metabolism. This dissociation of the responsiveness of insulin actions by fasting indicates that there may be at least two mechanisms of insulin resistance in the same cell.
Mol Cell Biochem 1981 Jul
PMID:Insulin resistance in adipocytes from fed and fasted obese rats: dissociation of two insulin actions. 727 60

The regulatory G-subunit of the glycogen-associated form of protein phosphatase 1 (PP1) plays a crucial part in muscle tissue glycogen synthesis and breakdown. As impaired insulin stimulated glycogen synthesis in peripheral tissues is considered to be a pathogenic factor in subsets of non-insulin-dependent diabetes mellitus (NIDDM) and obesity, the G-subunit of PP1 should be viewed as a candidate gene for inherited insulin resistance. When applying heteroduplex formation analysis and nucleotide sequencing of PP1G-subunit cDNA from 30 insulin resistant white NIDDM patients two cases were identified as heterozygous carriers of an Asp905 --> Tyr substitution. The carrier prevalence of the PP1G-subunit variant was 18% in 150 healthy subjects and 13% in 313 NIDDM subjects (chi 2 = 1.94, p = 0.16). Twenty-seven healthy subjects volunteered for a 4 h euglycaemic, hyperinsulinaemic clamp in combination with indirect calorimetry in order to elucidate the potential impact of the Tyr905 substitution on the whole body glucose metabolism. Interestingly, the Tyr905 variant was associated with altered routing of glucose: a decreased insulin stimulated non-oxidative glucose metabolism of peripheral tissues (glycogen synthesis) (p < 0.04) and an increased basal glucose oxidation rate (p < 0.04) when compared with wild type carriers. A population-based sample of 380 unrelated young healthy Caucasians was examined during a combined intravenous glucose and tolbutamide test to address whether the Asp905/Tyr905 polymorphism was associated with alterations in insulin secretion which might be secondary to the insulin resistance of skeletal muscle.(ABSTRACT TRUNCATED AT 250 WORDS)
Hum Mol Genet 1995 Aug
PMID:A widespread amino acid polymorphism at codon 905 of the glycogen-associated regulatory subunit of protein phosphatase-1 is associated with insulin resistance and hypersecretion of insulin. 758 68

Although sex steroids have long been known to influence serum concentrations of SHBG, it is now recognized that nutritional factors may be more important in the regulation of SHBG in women. Thus, SHBG concentrations are negatively correlated with body mass index (BMI) and, more particularly, to indices of central adiposity. Polycystic ovary syndrome (PCOS), the most common cause of anovulatory infertility, is associated with truncal obesity, hyperandrogenism and hyperinsulinaemia. There is evidence that insulin may be the humoral mediator of the weight-dependent changes in SHBG. Serum SHBG concentrations are inversely correlated with both fasting and glucose-stimulated insulin levels, and insulin has been shown to have a direct inhibitory effect on SHBG synthesis and secretion by hepatocytes in culture. However, the interrelationship of BMI, insulin and SHBG appears to be different in women with PCOS from that in normal subjects. The clinical importance of the weight-related suppression of SHBG is illustrated by the finding of a greater prevalence of hirsutism in obese women PCOS compared with their lean counterparts. Obese subjects with PCOS have similar total testosterone concentrations to lean PCO women but have lower SHBG and reciprocally higher free testosterone levels. Calorie restriction results in reduction of serum insulin followed by an increase in SHBG and a fall in free testosterone but an isocaloric, low-fat diet has no significant effect on SHBG concentrations. Weight reduction in obese, hyperandrogenaemic women with PCO is an important approach to the management of both anovulation and hirsutism.
J Steroid Biochem Mol Biol 1995 Jun
PMID:Sex hormone-binding globulin and female reproductive function. 762 5

Bardet-Biedl syndrome is a heterogeneous autosomal recessive disorder characterized by obesity, mental retardation, polydactyly, retinitis pigmentosa and hypogonadism. Patients with this disorder also have a high incidence of hypertension, diabetes mellitus, and renal and cardiovascular anomalies. Three independent loci causing Bardet-Biedl syndrome have previously been reported. In this study, we we utilized a DNA pooling approach using DNA samples from a highly inbred Bedouin kindred to identify a new Bardet-Biedl syndrome locus on chromosome 15. The results further demonstrate the genetic heterogeneity of this disorder. In addition, the results demonstrate the efficiency of the DNA pooling approach for identifying recessive disease loci in highly inbred human populations.
Hum Mol Genet 1995 Jan
PMID:Use of a DNA pooling strategy to identify a human obesity syndrome locus on chromosome 15. 771 39

The mouse agouti coat color gene encodes a novel paracrine signaling molecule whose pulsatile expression produces a characteristic pattern of banded pigment in individual hairs. Several spontaneous agouti alleles produce adult-onset obesity and diabetes, and have provided important single-gene animal models for alterations in energy metabolism. Utilizing linkage groups conserved between mice and humans, we have cloned the human homolog of the mouse agouti gene from a human chromosome 20 yeast artificial chromosome known to contain S-adenosyl homocysteine hydrolase (AHCY). The human agouti gene, named Agouti Signaling Protein (ASP), encodes a 132 amino acid protein, the mRNA for which is expressed in testis, ovary, and heart, and at lower levels in liver, kidney, and foreskin. As predicted by the interactions of mouse agouti with the extension gene (which encodes the melanocyte receptor for alpha-melanocyte stimulating hormone [alpha-MSH]), expression of ASP in transgenic mice produces a yellow coat, and expression of ASP in cell culture blocks the alpha-MSH-stimulated accumulation of cAMP in mouse melanoma cells. The localization of ASP relative to other loci on chromosome 20 excludes it as a candidate for the MODY1 locus, a gene responsible for one form of early-onset non-insulin-dependent diabetes mellitus or maturity-onset diabetes of the young. The expression of ASP in human tissues suggests a function for agouti homologs in species that do not exhibit the characteristic phenotype of banded hairs.
Hum Mol Genet 1995 Feb
PMID:Structure and function of ASP, the human homolog of the mouse agouti gene. 775 71

The mitochondrial FAD-linked enzyme glycerophosphate dehydrogenase plays a key role in the pancreatic B-cell glucose sensing device. In the present study, the activity of this enzyme was examined in islets of fa/fa rats in which inherited diabetes mellitus is associated with obesity, hyperinsulinism and severe insulin resistance. The specific activity of both FAD-linked glycerophosphate dehydrogenase and glutamate dehydrogenase were decreased in islet and liver homogenates prepared from fa/fa, as compared to Fa/Fa, rats, this coinciding with a low ratio between glutamateoxalacetate and glutamate-pyruvate transaminase activity in both islet and liver extracts, islet hyperplasia, hyperinsulinemia and hepatic steatosis in the hyperglycemic fa/fa rats. It is speculated that a low activity of FAD-linked glycerophosphate dehydrogenase in the pancreatic B-cell may participate to the perturbation of glucose homeostasis in fa/fa rats, like in other animal models of non-insulin-dependent diabetes mellitus.
Mol Cell Biochem 1994 Jun 29
PMID:Impaired FAD-glycerophosphate dehydrogenase activity in islet and liver homogenates of fa/fa rats. 783 41

The changes in alanine turnover were determined in Zucker rats, which were either genetically obese (fa/fa) or rendered obese by dietary treatment (cafeteria fed). The whole body rate of alanine turnover was higher in genetically obese rats than in rats in which obesity was induced by diet (cafeteria). This is possibly due to variations in the rate of the amino acid incorporation into proteins, since the rate of whole body alanine degradation is the same for both groups. Thus, the different pattern followed by alanine turnover rate in these types of obese animals reflects the differences in the nitrogen economy of these animals, pointing to a higher alanine utilization in the genetically obese animals and a conservative management of alanine in the cafeteria-fed animals.
Biochem Mol Biol Int 1994 Aug
PMID:Changes in alanine turnover rate due to nutritional and genetic obesity in the rat. 784 26

The study of intestinal and hepatic uptake of amino acids by obese rats has been the main objective of this work. The obese animals used were either from genetic or from nutritional basis. In fed state, the intestinal release of amino acids was higher in obese animals than in lean ones (around the double values), but nutritionally and genetically obese rat showed a related pattern, specially for the case of alanine (increased release in relation to controls by a factor of 10). The higher alanine release by intestine is not reversed by 12-h food deprivation. The hepatic availability was also higher in obesity models than in lean animals (increases over 30%). However, the hepatic uptake was increased in genetically obese animals (more than 35%) and decreased in nutritionally obese animals (more than 40%), especially due to alanine uptake (2419, 1100 and 3794 nmols/min/g protein in lean, Diet-ob and fa/fa animals respectively). In obese animals the food deprivation tended to normalize the hepatic uptake of alanine. The differences in alanine uptake between both types of obesity may reflect the differences of urea synthesis.
Mol Cell Biochem 1994 Oct 12
PMID:Splanchnic amino acid pattern in genetic and dietary obesity in the rat. 785 38


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