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  • NOD mouse  (2)
  • Prediabetes  (2)
  • 1,4-Dihydropyridine  (1)
  • Keywords Endogeneous insulin, hepatic glucose production, high protein diet, normal protein diet.  (1)
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  • 1
    ISSN: 0014-5793
    Keywords: 1,4-Dihydropyridine ; Ca^2^+-channel ; Skeletal muscle ; d-cis-[^3H]-diltiazem
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Keywords Endogeneous insulin, hepatic glucose production, high protein diet, normal protein diet.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. A meal rich in protein stimulates insulin secretion. Long-term effects of dietary protein on insulin release and glucose metabolism are, however, still not known. Our study focussed on the effect of different protein intake on pancreatic insulin secretion capacity, glycogen turnover and gluconeogenesis.¶Methods. Subjects with constant (6 months) dietary protein of 1.87 ± 0.26 g · kg–1· day–1 (1.25–2.41) named high protein group and with 0.74 ± 0.08 (0.57–0.80), normal protein group, were identified by a food questionnaire and were matched (n = 9) according to sex, age and calorie intake. They underwent an intravenous glucose tolerance test and a euglycaemic hyperinsulinaemic clamp with infusion of [6,6-2H2]-glucose combined with indirect calorimetry. To estimate net gluconeogenesis the usual diet was enriched by deuterated water or U-[13C6]-glucose and breath and plasma were sampled.¶Results. Glucose-stimulated insulin secretion was increased in the high protein group (516 ± 45 pmol/l vs 305 ± 32, p = 0.012) due to reduced glucose threshold of the endocrine beta cells (4.2 ± 0.5 mmol/l vs 4.9 ± 0.3, p = 0.031). Endogeneous glucose output was increased by 12 % (p = 0.009) at 40 pmol/l plasma insulin in the high protein group, but not at higher insulin concentration whereas overall glucose disposal was reduced. Fasting plasma glucagon was 34 % increased in the high protein group (p = 0.038). Fractional gluconeogenesis was increased by 40 % in subjects receiving a high protein diet as determined by both methods.¶Conclusion/interpretation. High protein diet is accompanied by increased stimulation of glucagon and insulin within the endocrine pancreas, high glycogen turnover and stimulation of gluconeogenesis. [Diabetologia (2000) 43: 1257–1265]
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-5233
    Keywords: Key words  Glucagon-like-peptide-1 ; Prediabetes ; NOD mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract   The effect of the insulinotropic gut hormone glucagon-like-peptide-1 (GLP-1) was studied on the residual insulin capacity of prediabetic nonobese diabetic (NOD) mice, a model of insulin-dependent diabetes mellitus (type 1). This was done using isolated pancreas perfusion and dynamic islet perifusion. Prediabetes was defined by insulitis and fasting normoglycemia. Insulitis occurred in 100% of NOD mice beyond the age of 12 weeks. K values in the intravenous glucose tolerance test were reduced in 20-week-old NOD mice compared with age-matched non-diabetes-prone NOR (nonobese resistant) mice (2.4±1.1 vs 3.8±1.5% min–1, P〈0.05). Prediabetic NOD pancreases were characterized by a complete loss of the glucose-induced first-phase insulin release. In perifused NOD islets GLP-1, at concentrations already effective in normal islets, left the insulin release unaltered. However, a significant rise of glucose-dependent insulin secretion occurred for GLP-1 concentrations 〉0.1 nM. This was obtained with both techniques, dynamic islet perifusion and isolated pancreas perfusion, indicating a direct effect of GLP-1 on the beta-cell. Analysis of glucose-insulin dose-response curves revealed a marked improvement of glucose sensitivity of the NOD endocrine pancreas in the presence of GLP-1 (half-maximal insulin output without GLP-1 15.2 mM and with GLP-1 9.4 mM, P〈0.002). We conclude that GLP-1 can successfully reverse the glucose sensing defect of islets affected by insulitis.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-5233
    Keywords: Glucagon-like-peptide-1 ; Prediabetes ; NOD mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of the insulinotropic gut hormone glucagon-like-peptide-1 (GLP-1) was studied on the residual insulin capacity of prediabetic nonobese diabetic (NOD) mice, a model of insulin-dependent diabetes mellitus (type 1). This was done using isolated pancreas perfusion and dynamic islet perifusion. Prediabetes was defined by insulitis and fasting normoglycemia. Insultis occurred in 100% of NOD mice beyond the age of 12 weeks. K values in the intravenous glucose tolerance test were reduced in 20-week-old NOD mice compared with agematched non-diabetes-prone NOR (nonobese resistant) mice (2.4±1.1 vs 3.8±1.5% min−1,P〈0.05). Prediabetic NOD pancreases were characterized by a complete loss of the glucose-induced first-phase insulin release. In perifused NOD islets GLP-1, at concentrations already effective in normal islets, left the insulin release unaltered. However, a significant rise of glucose-dependent insulin secretion occurred for GLP-1 concentrations〉0.1 nM. This was obtained with both techniques, dynamic islet perifusion and isolated pancreas perfusion, indicating a direct effect of GLP-1 on the beta-cell. Analysis of glucose-insulin dose-response curves revealed a marked improvement of glucose sensitivity of the NOD endocrine pancreas in the presence of GLP-1 (half-maximal insulin output without GLP-1 15.2 mM and with GLP-1 9.4 mM,P〈0.002). We conclude that GLP-1 can successfully reverse the glucose sensing defect of islets affected by insulitis.
    Type of Medium: Electronic Resource
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