

Journal of Health and Medical Sciences
ISSN 2622-7258







Published: 20 June 2022
Comparison of Effect of Exercise on Insulin Sensitivity of Overweight Normoglycemic Offspring of T2DM Parents and Non-Diabetic Parents
E. O. Taiwo, L. O. A. Thanni, A. Akinleye Waheed
Olabisi Onabanjo University, Nigeria

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10.31014/aior.1994.05.02.217
Pages: 93-98
Keywords: Diabetes Mellitus, Body Mass Index, Insulin Sensitivity, Offspring of Diabetes
Abstract
Background: The primary causes of Type 2 Diabetes Mellitus (T2DM) are largely unknown but insulin insensitivity has been reported to be a risk factor for the T2DM through the alteration of insulin sensitivity pattern. There is paucity of studies on the effect of exercise on occurrence of T2DM in offspring of diabetic parents in our population. Objectives: This study was designed to assess the effect of exercise on insulin sensitivity (IS) on offspring of T2DM parents compared with offspring of non-diabetic parents. Design: This study involved 60 offspring of T2DM parents attending University College Hospital, Ibadan and 60 offspring of non-diabetic parents who are undergraduate students of the University of Ibadan, Nigeria. Participants were randomly assigned into two groups. Each participant followed a protocol of graded exercise using ‘‘tummy trimmer’’ everyday spending 45 minutes daily for 24 weeks. Blood samples were obtained after an overnight fasting for determination of insulin sensitivity using standard methods at baseline and at 24 weeks. Data were analyzed using descriptive statistic and student t test with significance at p<0.05). Results: The most populated aged group was 26 to 35 years of which 47.3% (n=26) were OODP and 52.7% (n=29) were OONDP. However, all subjects were overweight with mean BMI of OODP and OONDP (29.30kg/m2±0.71 versus 26.37kg/m2±0.88) p=.0.035. Significantly, total insulin sensitivity between the two groups increased after 6 months of exercise p=0.045(3.36µ /l±0.24 versus 3.48µ /l±0.24). Conclusions: Male subjects tend to have higher insulin sensitivity than females.
References
Bacha F., Lee S., Gungor N., Arslanian S. (2010) From pre-diabetes to type 2 diabetes in obese youth: pathophysiological characteristics along the spectrum of glucose dysregulation. Diabetes Care 33: 2225-2231.
Narayan KM, Boyle JP, Thompson TJ, Gregg EW, Williamson DF. Effect of BMI on lifetime risk for diabetes in the US. Diabetes Care. 2007; 30:1562–6. [PubMed] [Google Scholar.
Jouret B, Ahluwalia N, Cristini C, Dupuy M, Nègre-Pages L, Grandjean H, et al. Factors associated with overweight in preschool-age children in south western France. Am J Clin Nutr. 2007; 85:1643–9. [PubMed] [Google Scholar]
Chathurvedi D, Khadgawat R, Kulshrestha B, Gupta N, Joseph AA, Diwedi S, et al. Type 2 diabetes increases risk for obesity among subsequent generations. Diabetes Technol Ther. 2009; 11: 393–8. [PubMed] [Google Scholar]
Meigs JB, Cupples LA, Wilson PW. Parental transmission of type 2 diabetes: The Framingham Offspring Study. Diabetes. 2000; 49:2201–7. [PubMed] [Google Scholar]
Shaw JT, Purdie DM, Neil HA, Levy JC, Turner RC. The relative risks of hyperglycaemia, obesity and dyslipidaemia in the relatives of patients with Type II diabetes mellitus. Diabetologia. 1999; 42: 24–7. [PubMed] [Google Scholar]
Natali A, Muscelli E, Mari A, Balkau B, Walker M, Tura A, et al. Relationship between insulin sensitivity and cardiovascular disease investigators: Insulin sensitivity and beta-cell function in the offspring of type 2 diabetic patients: Impact of line of inheritance. J Clin Endocrinol Metab. 2010; 95: 4703–11. [PubMed] [Google Scholar]
Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: Insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985; 28:412–9. [PubMed] [Google Scholar]
Radziuk J. Homeostastic model assessment and insulin sensitivity/resistance. Diabetes. 2014 Jun 1;63 (6):1850-4.
Pimenta W, Korytkowski M, Mitrakou A, Jenssen T, Yki-Jarvinen H, Evron W, et al. Pancreatic beta-cell dysfunction as the primary genetic lesion in NIDDM: Evidence from studies in normal glucose-tolerant individuals with a first-degree NIDDM relative. JAMA. 1995; 273:1855–61. [PubMed] [Google Scholar]
Van Haeften TW, Dubbel