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Journal ArticleDOI

Lilly lecture 1987. The triumvirate: beta-cell, muscle, liver. A collusion responsible for NIDDM.

Ralph A. DeFronzo
- 01 Jun 1988 - 
- Vol. 37, Iss: 6, pp 667-687
TLDR
Apres l'ingestion de glucose, l'insulino-secretion du pancreas est stimulee et la combinaison de l'hyperglycemie et de l-hyperinsulinemie doit induire la captation de glucose dans les territoires splanchique et peripherique (muscles) and the suppression of the production hepatique du glucose.
Abstract
Apres l'ingestion de glucose, l'insulino-secretion du pancreas est stimulee et la combinaison de l'hyperglycemie et de l'hyperinsulinemie doit induire la captation de glucose dans les territoires splanchique (foie et tube digestif) et peripherique (muscles) et la suppression de la production hepatique du glucose. Le but de cette conference est de prouver que, bien que la perturbation du metabolisme hepatique du glucose joue un role dans le maintien de l'etat diabetique, le foie ne joue probablement pas de role majeur dans le developpement precoce de l'hyperglycemie a jeun des DNID

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Citations
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C-Reactive Protein, Interleukin 6, and Risk of Developing Type 2 Diabetes Mellitus

TL;DR: Elevated levels of CRP and IL-6 predict the development of type 2 DM, and data support a possible role for inflammation in diabetogenesis.
Journal ArticleDOI

β-Cell Deficit and Increased β-Cell Apoptosis in Humans With Type 2 Diabetes

TL;DR: Since the major defect leading to a decrease in β-cell mass in type 2 diabetes is increased apoptosis, while new islet formation andβ-cell replication are normal, therapeutic approaches designed to arrest apoptosis could be a significant new development in the management of type 2 Diabetes.
Journal ArticleDOI

Follow-up report on the diagnosis of diabetes mellitus.

TL;DR: The International Expert Committee was convened to reexamine the classification and diagnostic criteria of diabetes, which were based on the 1979 publication of the National Diabetes Data Group and subsequent WHO study group and adopted several changes to the diagnostic criteria for diabetes and for lesser degrees of impaired glucose regulation (IFG/IGT).
Journal ArticleDOI

Quantitative insulin sensitivity check index: a simple, accurate method for assessing insulin sensitivity in humans.

TL;DR: It is concluded that QUICKI is an index of insulin sensitivity obtained from a fasting blood sample that may be useful for clinical research.
Journal ArticleDOI

Cellular mechanisms of insulin resistance

TL;DR: It is shown that commonly accepted models that attempt to explain the association of insulin resistance and obesity are incompatible with recent findings and an alternative model is proposed that appears to fit these and other available data.
References
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Journal ArticleDOI

Glucose clamp technique: a method for quantifying insulin secretion and resistance.

TL;DR: Methods for the quantification of beta-cell sensitivity to glucose (hyperglycemic clamp technique) and of tissue sensitivity to insulin (euglycemic insulin clamp technique] are described.
Journal ArticleDOI

The Effect of Insulin on the Disposal of Intravenous Glucose: Results from Indirect Calorimetry and Hepatic and Femoral Venous Catheterization

TL;DR: The results suggest that the ability of higher doses of insulin to further stimulate glucose metabolism is primarily the result of increased glucose storage by peripheral tissues, most likely muscle.
Journal ArticleDOI

Effects of insulin on peripheral and splanchnic glucose metabolism in noninsulin-dependent (type II) diabetes mellitus.

TL;DR: The results emphasize the importance of the peripheral tissues in the disposal of infused glucose and indicate that muscle is the most important site of the insulin resistance in NIDD.
Journal ArticleDOI

Effect of fatty acids on glucose production and utilization in man.

TL;DR: It is concluded that, in the well-insulinized state raised FFA levels effectively compete with glucose for uptake by peripheral tissues, regardless of the presence of hyperglycemia.
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