scholarly journals Heritability of Insulin Secretion, Peripheral and Hepatic Insulin Action, and Intracellular Glucose Partitioning in Young and Old Danish Twins

Diabetes ◽  
2004 ◽  
Vol 54 (1) ◽  
pp. 275-283 ◽  
Author(s):  
P. Poulsen ◽  
K. Levin ◽  
I. Petersen ◽  
K. Christensen ◽  
H. Beck-Nielsen ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Insulin Action ◽  
Glucose Partitioning ◽  
Intracellular Glucose

A Critical Review on Madhumeha (Diabetes Mellitus) with its Preventive Approach

2017 ◽  
Vol 2 (05) ◽  
Author(s):  
Anagha Gosavi ◽  
Ram V. Ramekar
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Secretion ◽  
Protein Metabolism ◽  
Insulin Action ◽  
Preventive Measures ◽  
Sweet Taste ◽  
Whole Body ◽  
Appropriate Use ◽  
Chronic Hyperglycemia ◽  
Therapeutic Measures

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.

scholarly journals Acute Alcohol Consumption Improves Insulin Action Without Affecting Insulin Secretion in Type 2 Diabetic Subjects

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 ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Alcohol Consumption ◽  
Insulin Action ◽  
Type 2 Diabetic

Antecedent protein restriction exacerbates development of impaired insulin action after high-fat feeding

1999 ◽  
Vol 276 (1) ◽  
pp. E85-E93 ◽  
Author(s):  
Mark J. Holness ◽  
Mary C. Sugden
Keyword(s):  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Insulin Action ◽  
Protein Restriction ◽  
Protein Diet ◽  
Glucose Disposal ◽  
High Fat ◽  
Impaired Insulin ◽  
Impaired Insulin Action ◽  
Fat Feeding

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.

Effect of benfluorex on insulin secretion and insulin action in streptozotocin-diabetic rats

1993 ◽  
Vol 9 (S1) ◽  
pp. 57S-63S ◽  
Author(s):  
Bernard Portha ◽  
Patricia Serradas ◽  
Danielle Bailbé ◽  
Olivier Blondel ◽  
Françoise Picarel
Keyword(s):  
Insulin Secretion ◽  
Insulin Action ◽  
Diabetic Rats ◽  
Streptozotocin Diabetic Rats

Insulin secretion and action and the response of endogenous glucose production to a lack of glucagon suppression in non-diabetic subjects

2021 ◽  
Author(s):  
Jon D Adams ◽  
Aoife M Egan ◽  
Marcello C Laurenti ◽  
Daniel J Schembri Wismayer ◽  
Kent R Bailey ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Insulin Action ◽  
Insulin Dose ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Oral Glucose ◽  
Prandial Insulin ◽  
Anthropometric Characteristics ◽  
Glucagon Suppression ◽  
Endogenous Glucose

Type 2 diabetes is a disease characterized by impaired insulin secretion and defective glucagon suppression in the postprandial period. We examined the effect of impaired glucagon suppression on glucose concentrations and Endogenous Glucose Production (EGP) at different degrees of insulin secretory impairment. The contribution of anthropometric characteristics, peripheral, and hepatic insulin action to this variability was also examined. To do so, we studied 54 non-diabetic subjects on two occasions in which endogenous hormone secretion was inhibited by somatostatin, with glucagon infused at a rate of 0.65 ng/kg/min, at 0 min to prevent a fall in glucagon (non-suppressed day) or at 120 min to create a transient fall in glucagon (suppressed day). Subjects received glucose (labeled with [3-3H]-glucose) infused to mimic the systemic appearance of 50g oral glucose. Insulin was infused to mimic a prandial insulin response in 18 subjects, another 18 received 80% of the dose and the remaining 18 received 60%. EGP was measured using the tracer-dilution technique. Decreased prandial insulin resulted in greater % increase in peak glucose but not in integrated glucose concentrations attributable to non-suppressed glucagon. The % change in integrated EGP was unaffected by insulin dose. Multivariate regression analysis, adjusted for age, sex, weight and insulin dose, did not show a relationship between the EGP response to impaired suppression of glucagon and insulin action as measured at the time of screening by oral glucose tolerance. A similar analysis for hepatic insulin action also did not show a relationship with the EGP response. These data indicate that the effect of impaired glucagon suppression on EGP is independent of anthropometric characteristics and insulin action.

scholarly journals Effect of early dietary restriction on insulin action and secretion in the GK rat, a spontaneous model of NIDDM

2000 ◽  
Vol 278 (6) ◽  
pp. E1097-E1103 ◽  
Author(s):  
Carmen Alvarez ◽  
Danielle Bailbe ◽  
Françoise Picarel-Blanchot ◽  
Eric Bertin ◽  
Ana-Maria Pascual-Leone ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Weight Gain ◽  
Glucose Tolerance ◽  
Glucose Uptake ◽  
Insulin Action ◽  
Food Restriction ◽  
Plasma Insulin ◽  
Insulin Level ◽  
Gk Rat ◽  
Basal Plasma

The availability of the Goto-Kakisaki (GK) rat model of non-insulin-dependent diabetes mellitus prompted us to test the effect of a limited period of undernutrition in previously diabetic young rats on their insulin secretion and insulin action during adult age. Four-week-old female GK rats were either food restricted (35% restriction, 15% protein diet) or protein and energy restricted (35% restriction, 5% protein diet) for 4 wk. Food restriction in the young GK rat lowered weight gain but did not aggravate basal hyperglycemia or glucose intolerance, despite a decrease in basal plasma insulin level. Furthermore, the insulin-mediated glucose uptake by peripheral tissues in the GK rat was clearly improved. We also found that food restriction, when it is coupled to overt protein deficiency in the young GK rat, altered weight gain more severely and slightly decreased basal hyperglycemia but conversely aggravated glucose tolerance. Improvement of basal hyperglycemia was related to repression of basal hepatic glucose hyperproduction, despite profound attenuation of basal plasma insulin level. Deterioration of tolerance to glucose was related to severe blunting of the residual glucose-induced insulin secretion. It is, however, likely that the important enhancement of the insulin-mediated glucose uptake helped to limit the deterioration of glucose tolerance.

scholarly journals The impact of dietary protein restriction on insulin secretion and action

1999 ◽  
Vol 58 (3) ◽  
pp. 647-653 ◽  
Author(s):  
Mark J. Holness
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Insulin Secretion ◽  
Insulin Action ◽  
Synergistic Effects ◽  
Protein Restriction ◽  
Dependent Diabetes Mellitus ◽  
Organ Systems ◽  
The Impact

The goal of this review is to develop the hypothesis, and review the evidence, that protein restriction, through synergistic effects on multiple organ systems predisposes to loss of normal regulation of fuel homeostasis that plays the central role in the development of type 2 (non-insulin-dependent) diabetes mellitus. The ability of insulin to regulate glucose production and disposal varies between individuals. These differences, together with the various compensatory mechanisms that are invoked to attempt to normalize fuel homeostasis, are of fundamental importance in the development and clinical course of type 2 diabetes mellitus. Protein deprivation impacts on both insulin secretion and insulin action. These effects may persist even when a diet containing adequate protein is presented subsequently. Data are presented that suggest that protein restriction results in an impaired ability of pancreatic β-cells to compensate adequately for the defect in insulin action in insulin-resistant individuals. This persistent impairment of insulin secretion resulting from protein restriction predisposes to loss of glucoregulatory control and impaired insulin action after the subsequent imposition of a diabetogenic challenge. This inability to maintain the degree of compensatory hyperinsulinaemia necessary to prevent loss of glucose tolerance may have relevance to the increased incidence of diabetes on changing from a nutritionally-poor diet to a Western diet, and to the hypothesis that some cases of type 2 diabetes in adulthood may be related to poor early nutrition.

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