scholarly journals Effect of 2 Years of Testosterone Replacement on Insulin Secretion, Insulin Action, Glucose Effectiveness, Hepatic Insulin Clearance, and Postprandial Glucose Turnover in Elderly Men

Diabetes Care ◽  
2007 ◽  
Vol 30 (8) ◽  
pp. 1972-1978 ◽  
Author(s):  
R. Basu ◽  
C. D. Man ◽  
M. Campioni ◽  
A. Basu ◽  
K. S. Nair ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Insulin Action ◽  
Postprandial Glucose ◽  
Insulin Clearance ◽  
Testosterone Replacement ◽  
Glucose Turnover ◽  
Elderly Men ◽  
Glucose Effectiveness ◽  
Hepatic Insulin Clearance

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 ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Insulin Action ◽  
Postprandial Glucose ◽  
Glucose Turnover ◽  
Elderly Men

scholarly journals Effects of Type 2 Diabetes on Insulin Secretion, Insulin Action, Glucose Effectiveness, and Postprandial Glucose Metabolism

Diabetes Care ◽  
2009 ◽  
Vol 32 (5) ◽  
pp. 866-872 ◽  
Author(s):  
A. Basu ◽  
C. Dalla Man ◽  
R. Basu ◽  
G. Toffolo ◽  
C. Cobelli ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Secretion ◽  
Glucose Metabolism ◽  
Insulin Action ◽  
Postprandial Glucose ◽  
Glucose Effectiveness

Effects of prolonged glucose infusion on insulin secretion, clearance, and action in normal subjects

1996 ◽  
Vol 270 (2) ◽  
pp. E251-E258 ◽  
Author(s):  
G. Boden ◽  
J. Ruiz ◽  
C. J. Kim ◽  
X. Chen
Keyword(s):  
Insulin Secretion ◽  
Plasma Glucose ◽  
Insulin Action ◽  
Human Subjects ◽  
Normal Subjects ◽  
Glucose Infusion ◽  
Insulin Clearance ◽  
Glucose Turnover ◽  
Peripheral Muscle ◽  
Muscle Insulin Action

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.

scholarly journals Hyperinsulinemia and Its Pivotal Role in Aging, Obesity, Type 2 Diabetes, Cardiovascular Disease and Cancer

2021 ◽  
Vol 22 (15) ◽  
pp. 7797
Author(s):  
Joseph A. M. J. L. Janssen
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Cardiovascular Disease ◽  
Insulin Secretion ◽  
Early Stage ◽  
Insulin Clearance ◽  
Future Research ◽  
Age Related ◽  
Hepatic Insulin Clearance

For many years, the dogma has been that insulin resistance precedes the development of hyperinsulinemia. However, recent data suggest a reverse order and place hyperinsulinemia mechanistically upstream of insulin resistance. Genetic background, consumption of the “modern” Western diet and over-nutrition may increase insulin secretion, decrease insulin pulses and/or reduce hepatic insulin clearance, thereby causing hyperinsulinemia. Hyperinsulinemia disturbs the balance of the insulin–GH–IGF axis and shifts the insulin : GH ratio towards insulin and away from GH. This insulin–GH shift promotes energy storage and lipid synthesis and hinders lipid breakdown, resulting in obesity due to higher fat accumulation and lower energy expenditure. Hyperinsulinemia is an important etiological factor in the development of metabolic syndrome, type 2 diabetes, cardiovascular disease, cancer and premature mortality. It has been further hypothesized that nutritionally driven insulin exposure controls the rate of mammalian aging. Interventions that normalize/reduce plasma insulin concentrations might play a key role in the prevention and treatment of age-related decline, obesity, type 2 diabetes, cardiovascular disease and cancer. Caloric restriction, increasing hepatic insulin clearance and maximizing insulin sensitivity are at present the three main strategies available for managing hyperinsulinemia. This may slow down age-related physiological decline and prevent age-related diseases. Drugs that reduce insulin (hyper) secretion, normalize pulsatile insulin secretion and/or increase hepatic insulin clearance may also have the potential to prevent or delay the progression of hyperinsulinemia-mediated diseases. Future research should focus on new strategies to minimize hyperinsulinemia at an early stage, aiming at successfully preventing and treating hyperinsulinemia-mediated diseases.

scholarly journals Hepatic Insulin Clearance: Mechanism and Physiology

Physiology ◽  
2019 ◽  
Vol 34 (3) ◽  
pp. 198-215 ◽  
Author(s):  
Sonia M. Najjar ◽  
Germán Perdomo
Keyword(s):  
Insulin Resistance ◽  
Insulin Secretion ◽  
Insulin Receptor ◽  
Hepatic Steatosis ◽  
Insulin Clearance ◽  
Hepatic Insulin Resistance ◽  
Insulin Degrading Enzyme ◽  
Insulin Receptor Tyrosine Kinase ◽  
Impaired Insulin ◽  
Hepatic Insulin Clearance

Upon its secretion from pancreatic β-cells, insulin reaches the liver through the portal circulation to exert its action and eventually undergo clearance in the hepatocytes. In addition to insulin secretion, hepatic insulin clearance regulates the homeostatic level of insulin that is required to reach peripheral insulin target tissues to elicit proper insulin action. Receptor-mediated insulin uptake followed by its degradation constitutes the basic mechanism of insulin clearance. Upon its phosphorylation by the insulin receptor tyrosine kinase, carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) takes part in the insulin-insulin receptor complex to increase the rate of its endocytosis and targeting to the degradation pathways. This review summarizes how this process is regulated and how it is associated with insulin-degrading enzyme in the liver. It also discusses the physiological implications of impaired hepatic insulin clearance: Whereas reduced insulin clearance cooperates with increased insulin secretion to compensate for insulin resistance, it can also cause hepatic insulin resistance. Because chronic hyperinsulinemia stimulates hepatic de novo lipogenesis, impaired insulin clearance also causes hepatic steatosis. Thus impaired insulin clearance can underlie the link between hepatic insulin resistance and hepatic steatosis. Delineating these regulatory pathways should lead to building more effective therapeutic strategies against metabolic syndrome.

Ethanol inhibits insulin action on lipolysis and on insulin release in elderly men

1993 ◽  
Vol 265 (2) ◽  
pp. E197-E202 ◽  
Author(s):  
G. Boden ◽  
X. Chen ◽  
R. A. DeSantis ◽  
Z. Kendrick
Keyword(s):  
Insulin Resistance ◽  
Stable Isotopes ◽  
Adipose Tissue ◽  
Insulin Secretion ◽  
Insulin Release ◽  
Insulin Action ◽  
Glucose Disposal ◽  
Elderly Men ◽  
C Peptide ◽  
Healthy Elderly

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.

Sign in / Sign up

Export Citation Format

Share Document