Journal ArticleDOI
The Banting Memorial Lecture 1971. Physiology of insulin in man.
TLDR
Insulin serves as the body's signal for the fed or fasted state, and certain metabolic states such as obesity or trauma alter the concentration of insulin at which no net transfer of fuel occurs, resulting in insulin resistance or hyper-sensitivity.Abstract:
Insulin serves as the body9s signal for the fed or fasted state. High insulin levels, the “fed” signal, initiate tissue uptake and storage of fuels. Low insulin levels, the “fasted” signal, initiate mobilization of stored fuels from tissue stores, the rate being proportional to the lowness of the insulin. Certain metabolic states such as obesity or trauma alter the concentration of insulin at which no net transfer of fuel occurs, resulting in insulin resistance or hyper-sensitivity.read more
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Journal ArticleDOI
Identification of a novel gene encoding an insulin-responsive glucose transporter protein
TL;DR: A cDNA has been cloned from a skeletal muscle library that encodes a novel glucose transporter protein exhibiting the following properties of an insulin-regulated hexose carrier protein: it is expressed exclusively in adipose tissue, skeletal muscle and heart, the principal organs with insulin-responsive glucose transport.
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Sequence of the human insulin gene
Graeme I. Bell,Raymond Pictet,William J. Rutter,Barbara Cordell,Edmund Tischer,Howard M. Goodman +5 more
TL;DR: A comparison of the human with the rat insulin genes indicates potential regulatory regions in the DNA segment preceding the gene and suggests that the ancestral form of the insulin gene had two intervening sequences.
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Somatostatin: Hypothalamic Inhibitor of the Endocrine Pancreas
Donna J. Koerker,Willy Ruch,Elliott W. Chideckel,Jerry P. Palmer,Charles J. Goodner,John W. Ensinck,Charles C. Gale +6 more
TL;DR: Somatostatin, a hypothalamic peptide that inhibits the secretion of pituitary growth hormone, inhibits basal insulin secretion infasted cats and rats and in fasted baboons both basal and arginine- stimulated secretion of insulin and glucagon are inhibited.
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Eating, exercise, and “thrifty” genotypes: connecting the dots toward an evolutionary understanding of modern chronic diseases
TL;DR: It is contended that the combination of continuous food abundance and physical inactivity eliminates the evolutionarily programmed biochemical cycles emanating from feast-famine and physical activity-rest cycles, which in turn abrogates the cycling of certain metabolic processes, ultimately resulting in metabolic derangements such as obesity and Type 2 diabetes.
Journal ArticleDOI
Insulin-Receptor Interaction in the Obese-Hyperglycemic Mouse: A MODEL OF INSULIN RESISTANCE
TL;DR: The decrease in insulin receptors in the ob/ob mouse correlates well with the insulin resistance which they exhibit and Scatchard analysis suggests that this decrease in binding is due to a decrease in the number of receptor sites in the membrane of the obese mouse, especially those of higher affinity.