scholarly journals Two Years of Treatment With Dehydroepiandrosterone Does Not Improve Insulin Secretion, Insulin Action, or Postprandial Glucose Turnover in Elderly Men or Women

Diabetes ◽  
2007 ◽  
Vol 56 (3) ◽  
pp. 753-766 ◽  
Author(s):  
R. Basu ◽  
C. Dalla Man ◽  
M. Campioni ◽  
A. Basu ◽  
K. S. Nair ◽  
...  
1993 ◽  
Vol 265 (2) ◽  
pp. E197-E202 ◽  
Author(s):  
G. Boden ◽  
X. Chen ◽  
R. A. DeSantis ◽  
Z. Kendrick

We have studied effects of ethanol on insulin's ability to suppress its own release and on its antilipolytic action in 12 healthy elderly men during euglycemic hyperinsulinemia. Insulin secretion was estimated from plasma C-peptide concentrations. Lipolysis was determined with the two stable isotopes [2H5]glycerol and [1-13C]palmitate. Hyperinsulinemia (approximately 350 pM) decreased plasma C-peptide by approximately 60% (from 325 to 122 pM, P < 0.05). Ethanol (approximately 10 mM) completely prevented the fall in C-peptide concentration. Ethanol decreased the antilipolytic action of insulin by approximately 40% [with insulin alone, glycerol rate of appearance (Ra) decreased from 1.8 to 0.6 mumol.kg-1 x min-1; with insulin + ethanol, it only decreased from 1.8 to 1.1 mumol.kg-1 x min-1]. Ethanol did not affect palmitate Ra, which fell from 1.4 to 0.6 mumol.kg-1 x min-1 with insulin and from 1.4 to 0.3 mumol.kg-1 x min-1 with insulin plus ethanol. Fatty acid reesterification was not affected by insulin but tripled (from 0.6 to 1.9 mumol.kg-1 x min-1) in response to insulin plus ethanol. Our data showed that modest concentrations of ethanol suppressed the inhibitory actions of insulin on its own release and on lipolysis. The inhibition by ethanol of various insulin actions, including glucose disposal, lipolysis, and insulin release, in diverse tissues such as muscle, adipose tissue, and pancreas raises the possibility that ethanol may produce a state of generalized insulin resistance.


Diabetes Care ◽  
2009 ◽  
Vol 32 (5) ◽  
pp. 866-872 ◽  
Author(s):  
A. Basu ◽  
C. Dalla Man ◽  
R. Basu ◽  
G. Toffolo ◽  
C. Cobelli ◽  
...  

1996 ◽  
Vol 270 (2) ◽  
pp. E251-E258 ◽  
Author(s):  
G. Boden ◽  
J. Ruiz ◽  
C. J. Kim ◽  
X. Chen

It was the aim of this study to determine whether prolonged hyperglycemia can produce "glucose toxicity" in normal human subjects. To this end, plasma glucose was clamped at approximately 5, approximately 8.8, and approximately 12.6 mM for 68 h in healthy volunteers. Rates of insulin secretion (by deconvolution of plasma C-peptide) and rates of insulin clearance [area under curve (AUC) 24 h insulin secretion/AUC 24 h insulin] were determined. Pre- and posthyperglycemia glucose turnover was measured (with [6,6-2H2]glucose) during euglycemic-hyperinsulinemic clamping to assess peripheral (muscle) and hepatic insulin action. Hyperglycemia (approximately 12.6 mM) for 68 h was associated with significant reductions in rates of insulin secretion (-35%, P < 0.05), insulin clearance (-57%, P < 0.05), glucose infusion rates needed to maintain hyperglycemia (-36%, P < 0.05), and insulin-stimulated glucose uptake (-55%, P < 0.01). No significant changes were seen during approximately 8.8 mM hyperglycemia or during euglycemia. These data showed that 12.6 mM hyperglycemia, but not 8.8 mM hyperglycemia or euglycemia, was associated with reduced insulin secretion, insulin clearance, and peripheral (muscle) insulin action. We concluded that 1) in normal subjects, desensitization to glucose involving beta-cells and muscle developed at plasma glucose concentrations between approximately 9 and approximately 12 mM, and 2) these effects were partially compensated for by a decrease in insulin clearance.


Author(s):  
Anagha Gosavi ◽  
Ram V. Ramekar

Prameha is disease of Mutravaha Srotasa having Kapha dominancy which can be correlated with diabetes mellitus. The term diabetes mellitus describes a metabolic disorder of multiple etiologies characterized by chronic hyperglycemia with disturbances of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion, insulin action, or both. Madhumeha is considered as a subtype under the Vatika type of Prameha and it is characterized by passage of urine with sweet taste like honey along with sweetness of whole body. With appropriate use of Ayurvedic preventive measures such as Dincharya, Ritucharya, Aharvidhi and therapeutic measures Madhumeha (DM) can be prevented.


Diabetes Care ◽  
2004 ◽  
Vol 27 (6) ◽  
pp. 1369-1374 ◽  
Author(s):  
A. Avogaro ◽  
R. M. Watanabe ◽  
A. Dall'Arche ◽  
S. Vigili De Kreutzenberg ◽  
A. Tiengo ◽  
...  

1999 ◽  
Vol 276 (1) ◽  
pp. E85-E93 ◽  
Author(s):  
Mark J. Holness ◽  
Mary C. Sugden

The study investigated whether a persistent impairment of insulin secretion resulting from mild protein restriction predisposes to loss of glucoregulatory control and impaired insulin action after the subsequent imposition of the diabetogenic challenge of high-fat feeding. Offspring of dams provided with either control (20% protein) diet (C) or an isocaloric restricted (8%) protein diet (PR) were weaned onto the maintenance diet with which their mothers had been provided. At 20 wk of age, protein restriction enhanced glucose tolerance despite impaired insulin secretion and an augmented and sensitized lipolytic response to norepinephrine in adipocytes. C and PR rats were then transferred to a high-fat diet (HF, 19% protein, 22% lipid, 34% carbohydrate) and sampled after 8 wk. These groups are termed C-HF and PR-HF. Glucose tolerance was impaired in PR-HF, but not C-HF, rats. Insulin-stimulated glucose disposal rates were significantly lower (by 30%; P < 0.01) in the PR-HF group than in the C-HF group, and a specific impairment of antilipolytic response of insulin was unmasked in adipocytes from PR-HF, but not C-HF, rats. The study demonstrates that antecedent protein restriction accelerates and augments the development of impaired glucoregulation and insulin resistance after high-fat feeding.


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