scholarly journals A STUDY ON EFFECT OF DRUG DURING IN CLINICAL MANAGEMENT OF DIABETES

Author(s):  
Khushboo ◽  
Yogesh Sharma

Diabetes is defined as a state in which homeostasis of carbohydrate, protein and lipid metabolism is improperly regulated as a consequence of a relative or absolute deficiency of insulin secretion, resistance to insulin action or both at one or more center in tedious pathways of hormones activity. Diabetes is deadly disease in both developed and developing countries. In 2000, there were a probable 175 million people with diabetes universal and by 2030, the projected estimate of diabetes is 354 million. The most widely recognized unfavorable responses to insulin are weight addition and hypoglycaemia (Henry et al, 1993; Kudlacek et al, 1992). Weight increase in the wake of beginning insulin treatment for uncontrolled diabetes is an inescapable outcome and is the consequence of expanded truncal fat and muscle mass and severe side effects of biguanides include diarrhoea, abdominal discomfort, nausea, metallic taste, and anorexia. Keywords: Diabetes, Insulin, Biguanides and Hypoglycaemia

Diabetes ◽  
1985 ◽  
Vol 34 (3) ◽  
pp. 222-234 ◽  
Author(s):  
W. T. Garvey ◽  
J. M. Olefsky ◽  
J. Griffin ◽  
R. F. Hamman ◽  
O. G. Kolterman

Diabetes ◽  
1985 ◽  
Vol 34 (3) ◽  
pp. 222-234 ◽  
Author(s):  
W. T. Garvey ◽  
J. M. Olefsky ◽  
J. Griffin ◽  
R. F. Hamman ◽  
O. G. Kolterman

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.


1993 ◽  
Vol 9 (S1) ◽  
pp. 57S-63S ◽  
Author(s):  
Bernard Portha ◽  
Patricia Serradas ◽  
Danielle Bailbé ◽  
Olivier Blondel ◽  
Françoise Picarel

Author(s):  
Jon D Adams ◽  
Aoife M Egan ◽  
Marcello C Laurenti ◽  
Daniel J Schembri Wismayer ◽  
Kent R Bailey ◽  
...  

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.


2000 ◽  
Vol 278 (6) ◽  
pp. E1097-E1103 ◽  
Author(s):  
Carmen Alvarez ◽  
Danielle Bailbe ◽  
Françoise Picarel-Blanchot ◽  
Eric Bertin ◽  
Ana-Maria Pascual-Leone ◽  
...  

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.


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