Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunoreactive glucagon (IRG) response to a 3 min iv infusion of 25 g glucose was examined in 7 nondiabetic Caucasians, 8 nondiabetic, 8 prediabetic and 16 diabetic Pima Indians to define the normal IRG response and to determine if abnormalities of IRG suppression occur in diabetic and prediabetic Pima Indians. Fasting IRG levels were similar in the 3 nondiabetic groups. In response to the glucose infusion the maximum percentage fall in plasma IRG concentration was similar in the normal Caucasians (37+/-4%) and the normal (42+/-2%) and prediabetic Indians (43+/-3%). In the diabetic Indians the relative fall was less at all sampling times than among the prediabetic or normal Indians. No evidence of any differences in IRG suppression in prediabetic and normal Indians or normal Caucasians was found. Without detectable change in insulin levels during the first 10 min following the glucose infusion, IRG levels in the diabetics fell but to a lesser degree than that in the other groups.
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PMID:Immunoreactive glucagon (IRG) responses to intravenous glucose in prediabetes and diabetes among Pima Indians and normal Caucasians. 87 May 19

To determine whether abnormalities in glucagon secretion might precede the onset of hyperglycemia in diabetes mellitus, 32 prediabetic Pima (American) Indians, 27 normal Pima Indians and 34 normal Caucasians received an infusion of arginine monochloride (5 mg/kg/min for 40 minutes) with measurement of glucose, insulin, and glucagon. [Prediabetes is the period between conception and the development of diabetes. In most studies the term is used to characterize patients who on genetic grounds are believed to be at high risk of developing the disease, including the normoglycemic monozygotic co-twin of a diabetic or the normoglycemic offspring of two diabetic parents. The latter definition is used in the present study recognizing that in the final analysis the true prediabetic can be identified only in retrospect after the development of diabetes.] The three groups had similar mean fasting glucagon levels. During arginine infusion, the prediabetic Indians reached a mean maximum glucagon level of 315 +/- 14 pg/ml (mean +/- 1 SEM) compared with 294 +/- 20 pg/ml in the normal Indians and 292 +/- 25 pg/ml in the normal Caucasians. The calculated mean areas above baseline under the glucagon curves were 5704 +/- 324 pg-min/ml in the prediabetics, 5189 +/- 446 pg-min/ml in the normal Indians, and 4239 +/- 613 pg/min/ml in the normal Caucasians. The differences among the groups in these variables were not statistically significant. Thus, arginine induced hyperglucagonemia could not be identified as a characteristic of the prediabetic state in Pima Indians.
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PMID:Normal glucagon response to arginine infusion in "prediabetic" Pima Indians. 95 Mar 63

Groups of 27 nondiabetic Pima Indians, 34 nondiabetic Caucasians, and 12 diabetic Pima Indians with recent onset of their disease received an arginine infusion to determine if (1) nondiabetic Pima Indians and Caucasians had a similar glucagon response to arginine and (2) diabetic Pimas had excessive glucagon response to arginine as reported in other racial groups. The fasting glucagon levels in the three groups were not significantly different. During arginine monochloride infusion (5 mg./kg./minute for 40 minutes) the diabetic Pimas had glucagon levels significantly higher at 10 minutes and at all sampling points thereafter than the normo-glycemic Pimas. Plasma insulin levels also increased during the infusion but, notably, never differed significantly between these two groups. There was no significant difference in the glucagon levels at any sampling point between the nondiabetic Pimas and Caucasians. The differences in glucagon levels between the nondiabetic and diabetic Indians are similar to those differences reported between diabetic and nondiabetic subjects of other racial origins.
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PMID:Arginine-stimulated hyperglucagonemia in diabetic Pima Indians. 126 39

As part of an ongoing search for diabetes susceptibility loci, we tested linkage with non-insulin-dependent diabetes mellitus (NIDDM) for 19 candidate loci or regions chosen for their potential to affect directly or indirectly the action of insulin. Loci were associated with insulin resistance, known effects on lipid metabolism, or effects on glucose metabolism or insulin action. Loci included the insulin-responsive (GLUT4) glucose transporter, hexokinase 2, glucagon, growth hormone, insulin receptor substrate 1 (IRS1), phosphoenolpyruvate carboxykinase, hepatic and muscle forms of pyruvate kinase, hepatic phosphofructokinase, the apolipoprotein B and the apolipoprotein A2 cluster, lipoprotein lipase, hepatic triglyceride lipase, the very-low-density-lipoprotein receptor, and the Pima insulin resistance locus on chromosome 4. For several candidates, no specific informative marker was available; consequently, we tested the surrounding region with highly informative markers. These regions included the diabetes-associated ras-like gene, rad, and the cholesterol ester-transfer gene, both mapped to chromosome 16. Additionally, we tested for linkage with markers at the tumor necrosis factor-alpha gene and the Friedreich's ataxia region. All regions were tested for linkage with microsatellite polymorphisms in > 450 individuals from a minimum of 16 Caucasian families under parametric (LINKAGE 5.1) and nonparametric (affected pedigree member) models.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Linkage analysis of 19 candidate regions for insulin resistance in familial NIDDM. 758 21

The aim of this work was to study the effects of a computer-driven mental arithmetic task on blood glucose in a group of four male and four female euglycemic Caucasians and a group of seven male and six female euglycemic Pima Indians. Approximately 60% of euglycemic Pima Indian Native Americans eventually develop type 2 diabetes, while only 5% of Caucasians develop the disease. All subjects had normal glucose tolerance. Subjects were given a standard breakfast; 2 h later, they were given a computerized mental arithmetic stress test for 10 min. Before, during and after the test, several variables were analyzed, including serum concentrations of glucose, insulin, glucagon and plasma cortisol and catecholamines. Heart rate, systolic and diastolic blood pressure and all the stress hormones increased during stress and decreased during recovery in all subjects. Blood glucose consistently declined one hour after the meal in all subjects. However, while it continued to decline following stress in seven out of eight Caucasian subjects, it consistently increased during and following stress in 10 out of 13 Pima Indians. Fasting serum glucose in Pima Indians and Caucasians was respectively 5.07 + 0.08 mM and 5.04 + 0.09 mM. Two-hour post-prandial values were 5.63 + 0.22 mM and 5.48 + 0.19 mM respectively, whereas post-stress values were 6.15 + 0.19 mM for Pima Indians and 5.22 + 0.20 mM for Caucasians. Both serum glucose means following stress (t = 3.1, P < 0.005) and the direction of change in serum glucose in response to mental arithmetic (chi 2 = 8.2, P < 0.01) clearly differentiated Pimas from Caucasians.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glycemic response to stress is altered in euglycemic Pima Indians. 786 78