Monitoring of Patient With Diabetes Mellitus

Diabetes mellitus is a disease characterized by hyperglycemia, which is caused by impaired insulin secretion, impaired insulin action, or both. Chronic hyperglycemia will lead to dysfunction and damage to various organs, such as the eyes, kidneys, nerves, heart, and blood vessels. This paper discusses the monitoring of patients with diabetes mellitus according to the laboratory tests, to know when the results of therapy has reached the optimum point as well as the prevention of complications that can occur.

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

Journal of Ayurveda and Integrated Medical Sciences (JAIMS) ◽

10.21760/jaims.v2i05.10259 ◽

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.

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

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1999.276.1.e85 ◽

1999 ◽

Vol 276 (1) ◽

pp. E85-E93 ◽

Cited By ~ 18

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.

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059. POOR GROWTH BEFORE BIRTH IMPAIRS INSULIN SECRETION - WHAT WE HAVE LEARNT ABOUT THE MECHANISMS FROM THE PLACENTALLY-RESTRICTED SHEEP

Reproduction Fertility and Development ◽

10.1071/srb09abs059 ◽

2009 ◽

Vol 21 (9) ◽

pp. 14

Author(s):

K. L. Gatford

Keyword(s):

Insulin Resistance ◽

Insulin Secretion ◽

Beta Cell ◽

Insulin Action ◽

Cell Function ◽

Cell Mass ◽

Beta Cell Mass ◽

Poor Growth ◽

Impaired Insulin ◽

Impaired Insulin Action

Diabetes occurs when insulin secretion fails to increase sufficiently to compensate for developing insulin resistance. This implies that the increased risk of diabetes in adults who were small at birth reflects impaired insulin secretion as well as their well-known insulin resistance. More recently, direct evidence has been obtained that adults and children who were growth-restricted before birth secrete less insulin than they should, given their level of insulin resistance. Our research group is using the placentally-restricted (PR) sheep to investigate the mechanisms underlying impaired insulin action (sensitivity and secretion) induced by poor growth before birth. Like the intra-uterine growth-restricted (IUGR) human, the PR sheep develops impaired insulin action by adulthood, but has enhanced insulin sensitivity in infancy, associated with neonatal catch-up growth1, 2. Impaired insulin action begins to develop in early postnatal life, where although basal insulin action is high due to enhanced insulin sensitivity, maximal glucose-stimulated insulin action is already impaired in males3. Our cellular and molecular studies have identified impaired beta-cell function rather than mass as the likely cause of impaired insulin secretion, and we have reported a novel molecular defect in the calcium channels involved in the insulin secretion pathway in the pancreas of these lambs3. Upregulation of IGF-II and insulin receptor are implicated as key molecular regulators of beta-cell mass in the PR lamb3. By adulthood, both basal and maximal insulin action are profoundly impaired in the male lamb who was growth-restricted at birth2. These studies suggest therapies to prevent diabetes in the individual who grew poorly before birth should target beta-cell function, possibly in addition to further increasing beta-cell mass, to improve insulin secretion capacity, and its ability to increase in response to development of insulin resistance. We are now using the PR sheep to test potential therapies, since the timing of pancreatic development and hence exposure to a growth-restricting environment, is similar to that of the human.

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