MEDSYNC Inc.
About:
Type 2 diabetes primarily
develops from pathogenic defects in the mechanisms of insulin secretion and
hepatic and peripheral insulin action. The consequent disruption of normal
glucose metabolism involves a number of organ systems and is ultimately
manifested in fasting and daytime hyperglycemia. Chronically elevated blood
glucose concentrations determine the progression of the disease by further
exacerbating insulin resistance and causing beta-cell exhaustion in addition to
decreasing their responsiveness to glucose. The beta-cell secretory dysfunction
is characterized by the lack of the early phase of glucose-induced insulin secretion
and the insufficient and delayed late phase of secretion. Glycemic levels in
patients with type 2 diabetes are directly related to the risk of developing
microvascular and macrovascular complications, the main cause of the morbidity
and mortality associated with this disease. The goal of treatment is to
decrease the risk and delay the progression of these complications by improving
glycemic control.
Current oral antidiabetic
agents, used as monotherapy or in combination, include traditional insulin
secretagogues, insulin sensitizers and inhibitors of carbohydrate absorption. A
greater understanding of the pathophysiology of type 2 diabetes and recent
findings on the significance of meal-related glycemia to overall glycemic
control are expanding the therapeutic options for treating this disease. A
number of clinical tests have been developed to assess insulin sensitivity and
beta cell function in vivo. Early diagnosis of insulin resistance at the early
stage of disease is a prerequisite for effective prevention of its unfavorable
sequelae, including reduction of cardiovascular morbidity and mortality. In
1985 a homeostatic model was developed for the assessment of insulin resistance
aka HOMA. It was based on feedback dependence between fasting serum concentrations
of insulin and glucose in blood and correlated well with data obtained using
the isoglycemic glucose clamp. This program is based on the derivations of
those studies.
Installation:
Simply hotsync the file HOMA.prc
to your PDA.
Modules:
These programs can be
directly accessed from HOMA but you need to have them loaded on your PDA first.
Download them from HERE:
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Disclaimer:
This program is intended for
education purposes only. Please be sure that you have read the literature
completely before attempting to apply this program to anyone. Using this
program is at YOUR discretion only and YOU bear the responsibility of its use.
Support:
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Contact:
References:
1.
Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. 1985 Homeostasis model
assessment: insulin resistance and beta-cell function from fasting plasma
glucose and insulin concentrations in man. Diabetologia. 28:412-419
2.
Levy JC, Matthews DR, Hermans MP. 1998 Correct homeostasis model assessment (HOMA)
evaluation uses the computer program. Diabetes Care. 21:2191-2192.