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  • Electronic Resource  (4)
  • Cholesterol  (2)
  • NOD mouse  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Glucagon-like-peptide-1 (7–36) amide improves glucose sensitivity in beta-cells of NOD mice (1996)
    Springer
    Acta diabetologica 33 (1996), S. 19-24 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00571935
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Glucagon-like-peptide-1 (7–36) amide improves glucose sensitivity in beta-cells of NOD mice (1996)
    Springer
    Acta diabetologica 33 (1996), S. 19-24 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00571935
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Failure to reduce cholesterol as explanation for the limited efficacy of antihypertensive treatment in the reduction of CHD (1987)
    Springer
    Journal of molecular medicine 65 (1987), S. 828-832 
    Details
    ISSN: 1432-1440
    Keywords: Cholesterol ; Intervention ; Hypertension ; CHD reduction ; Trials
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Over the past 6 years, major hypertension intervention studies in Europe, Australia, and the USA have shown disappointing results in the prevention of coronary heart disease (CHD) in spite of adequate treatment and good compliance. Recently, it has become increasingly clear that hypertensives with or without treatment display higher cholesterol levels than normotensive persons. The present review examines cholesterol levels in six intervention studies, none of which offered dietary or drug therapy for hypercholesterolemic patients. The Oslo study and the British MRC Trial reported very high average cholesterol levels and both showed no protection from CHD through intensive therapy in comparison to control patients. The Australian and the American MRFIT studies produced evidence for reduced coronary mortality among hypertensives with low in contrast to those with high cholesterol levels. The European Working Party showed indirectly that patients with marked reduction in blood pressureand cholesteral had a significantly lower cardiac mortality compared to placebo-treated patients. The IPPPSH study found that increasing cholesterol levels in hypertensives under beta blockeror diuretic therapy increased the risk of myocardial infarction. Failure to reduce cholesterol in hypertensive patients apparently is a major reason for the limited efficacy of antihypertensive treatment in the reduction of CHD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01727479
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    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Influence of dietary sodium restriction on lipid metabolism (1993)
    Springer
    Journal of molecular medicine 71 (1993), S. 990-992 
    Details
    ISSN: 1432-1440
    Keywords: Salt restriction ; Lipoproteins ; Cholesterol ; Obesity ; Hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The possible increase in total and low-density lipoprotein cholesterol following severe restriction of dietary NaCl was reported in 1990 and and 1991 from three experiments, one in the United States and two in Germany. Each of these experiments lasted only 1 week. To evaluate the clinical side effects we analyzed data collected from patients who completed a course of NaCl-restricted weight reduction at the Duke Diet and Fitness Center. Observations of lipid changes are not available for periods of less than 3 weeks; however, we were able to collect data on lipid and lipoprotein changes from 556 participants 25 days after they were referred for weight reduction. Total cholesterol, low-density lipoprotein cholesterol, and triglyceride levels returned to normal in the majority of obese patients. In our slightly longer observation period in patients on a 1000 mg NaCl restricted diet we found no evidence of hyperlipidemic side effects. We believe that the hyperlipidemia resulting from severe sodium restriction in non-hypertensive, normal-weight individuals is not relevant to the problem of nonpharmacological and diuretic treatment of obese hypertensive patients. In clinically healthy, normal-weight, normotensive individuals severe salt restriction serves no practical or therapeutic purpose.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00180029
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    Paper (German National Licenses)
    Fulltext
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