A Study of BMI and Parasympathetic Functions in Healthy Offsprings of Type 2 Diabetes Mellitus
Journal Title: International Physiology - Year 2018, Vol 6, Issue 1
Abstract
Objective: Diabetes Mellitus is a group of common metabolic disorders that share the phenotype of hyperglycemia. Several distinct types of Diabetes Mellitus exist and are caused by interaction of genetics and environmental factors. Individuals with Diabetes Mellitus may develop signs of autonomic dysfunction involving cholinergic, noradrenergic and peptidergic systems. Type 2 Diabetes Mellitus has a strong genetic component. Individuals with a parent with Type 2 Diabetes Mellitus have an increased risk of Diabetes. If both parents have Type 2 Diabetes Mellitus, the risk approaches to 40%. Thus this study is designed to evaluate BMI and autonomic functions in nondiabetic offsprings of Type 2 diabetic parents. Method: The cross-sectional study of BMI and Parasympathetic Functions was carried out in 30 healthy offsprings of Type 2 Diabetic Parents (Study group) and 30 healthy offsprings of Nondiabetic Parents (Control group) in the age range of 18 - 21 years randomly selected among 1st MBBS students. Statistical Analysis is done by ‘Z’ test. Results: There is insignificant decrease in parasympathetic functions and insignificant increase in BMI in Study Group compared to Control Group. Conclusion: Our observations indicate that subclinical autonomic dysfunction may develop without the presence of long-term hyperglycemia in family members of Type 2 diabetic subjects having higher BMI; Thus, it is not simply a complication of the hyperglycemia in these patients. An explanation could be that it is possible to inherit susceptibility genes for autonomic neuropathy, and that these genes could be expressed before or maybe even without the subjects developing diabetes. Different factors (including hyperglycemia) could subsequently affect the expression of the genes and influence the progression of neuropathy.
Authors and Affiliations
Sangeeta Dattatreya Tuppad
Keywords
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- EP ID EP584872
- DOI 10.21088/ip.2347.1506.6118.6
- Views 76
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