Functional activity of the adrenal glands and abdominal obesity index as markers of dyslipidemia in patients with diabetes mellitus type 2
Keywords:obesity, diabetes mellitus type 2, corticosteroids, cortisol, DHEA, visceral obesity index, dyslipidemia
Cortisol and DHEA disbalance that appears in patients with diabetes mellitus type 2 leads to certain metabolic changes especially hyperglycemia, dyslipidemia, accumulation of abdominal fats, increase of proteins decay.
Aim. The study of correlations between cortisol/DHEA ratio, constitutional parameters (degree of obesity, character of fat distribution), abdominal obesity index, rates of blood lipid spectrum in patients with diabetes mellitus (DM) type 2.
Methods. For this aim there were examined 19 patients with DM type 2. There were used general clinical (body mass, height, waist and hips size, body mass and visceral obesity indices), biochemical (glycemia level, blood serum lipid spectrum rates), hormonal (C-peptide, cortisol, dehydroepiandrosterone sulfate) and statistical (Student criterion) methods of research.
Results. There was established that increase of cortisol/DHEA ratio rate is followed with growth of glycemia and glycated hemoglobin ( HbA1c) levels and also has a negative influence on blood serum lipid spectrum, that is favors an increase of triglycerindes, atherogenic fractions of cholesterol lipoproteins of the low density (LPLD) and lipoproteins of the very low density (LPVLD) concentration, decrease of anti-atherogenic lipoproteins of the high density (LPHD) content at the stable C-peptide level. The aforesaid negative processes took place simultaneously with the changes of visceral obesity index (VOI) that includes both the character of distribution and the function of adipose tissue.
Conclusion. Calculation of VOI in patients with diabetes mellitus type 2 as the marker of lipid metabolism disorder and stress/anti-stress corticosteroid disbalance is useful and reasonable
Geetha, L., Deepa, M., Anjana, R. M., Mohan, V. (2011). Prevalence and Clinical Profile of Metabolic Obesity and Phenotypic Obesity in Asian Indians. Journal of Diabetes Science and Technology, 5 (2), 439–446. doi: 10.1177/193229681100500235
Reaven, G. M. (1988). Banting lecture 1988. Role of insulin resistance in human disease. Diabetes, 37 (12), 1595–1607. doi: 10.2337/diabetes.37.12.1595
Savineau, J.-P., Marthan, R., Dumas de la Roque, E. (2013). Role of DHEA in cardiovascular diseases. Biochemical Pharmacology, 85 (6), 718–726. doi: 10.1016/j.bcp.2012.12.004
Tchernof, A., Labrie, F. (2004). Dehydroepiandrosterone, obesity and cardiovascular disease risk: a review of human studies. European Journal of Endocrinology, 151 (1), 1–14. doi: 10.1530/eje.0.1510001
Traish, A. M., Kang, H. P., Saad, F., Guay, A. T. (2011). Dehydroepiandrosterone (DHEA)-A Precursor Steroid or an Active Hormone in Human Physiology (CME). The Journal of Sexual Medicine, 8 (11), 2960–2982. doi: 10.1111/j.1743-6109.2011.02523.x
Phillips, A. C., Carroll, D., Gale, C. R., Lord, J. M., Arlt, W., Batty, G. D. (2010). Cortisol, DHEA sulphate, their ratio, and all-cause and cause-specific mortality in the Vietnam Experience Study. European Journal of Endocrinology, 163(2), 285–292. doi: 10.1530/eje-10-0299
Djurhuus, C. B., Gravholt, C. H., Nielsen, S., Mengel, A., Christiansen, J. S., Schmitz, O. E., Møller, N. (2002). Effects of cortisol on lipolysis and regional interstitial glycerol levels in humans. American Journal of Physiology – Endocrinology And Metabolism, 283 (1), E172–E177. doi: 10.1152/ajpendo.00544.2001
Gross, K. L., Cidlowski, J. A. (2008). Tissue-specific glucocorticoid action: a family affair. Trends in Endocrinology & Metabolism, 19 (9), 331–339. doi: 10.1016/j.tem.2008.07.009
Hughes, K. A., Manolopoulos, K. N., Iqbal, J., Cruden, N. L., Stimson, R. H., Reynolds, R. M. et. al (2012). Recycling Between Cortisol and Cortisone in Human Splanchnic, Subcutaneous Adipose, and Skeletal Muscle Tissues In Vivo. Diabetes, 61 (6), 1357–1364. doi: 10.2337/db11-1345
Kollind, M., Adamson, U., Lins, P., Efendic, S. (1987). Diabetogenic Action of GH and Cortisol in Insulin-Dependent Diabetes Mellitus Aspects of the Mechanisms Behind the Somogyi Phenomenon. Hormone and Metabolic Research, 19 (04), 156–159. doi: 10.1055/s-2007-1011766
Whitworth, J. A., Mangos, G. J., Kelly, J. J. (2000). Cushing, Cortisol, and Cardiovascular Disease. Hypertension, 36 (5), 912–916. doi: 10.1161/01.hyp.36.5.912
Lefebvre, P. (2006). Sorting out the roles of PPAR in energy metabolism and vascular homeostasis. Journal of Clinical Investigation, 116 (3), 571–580. doi: 10.1172/jci27989
Semple, R. K. (2006). PPAR and human metabolic disease. Journal of Clinical Investigation, 116 (3), 581–589. doi: 10.1172/jci28003
Unger, R. H. (2001). Diseases of liporegulation: new perspective on obesity and related disorders. The FASEB Journal, 15 (2), 312–321. doi: 10.1096/fj.00-0590
Samaras, N., Samaras, D., Frangos, E., Forster, A., Philippe, J. (2013). A Review of Age-Related Dehydroepiandrosterone Decline and Its Association with Well-Known Geriatric Syndromes: Is Treatment Beneficial? Rejuvenation Research, 16 (4), 285–294. doi: 10.1089/rej.2013.1425
Davis, S. R., Shah, S. M., McKenzie, D. P., Kulkarni, J., Davison, S. L., Bell, R. J. (2008). Dehydroepiandrosterone Sulfate Levels Are Associated with More Favorable Cognitive Function in Women. The Journal of Clinical Endocrinology & Metabolism, 93 (3), 801–808. doi: 10.1210/jc.2007-2128
Weiss, E., Villareal, D. T., Fontana, L., Han, D.-H., Holloszy, J. O. (2011). Dehydroepiandrosterone (DHEA) replacement decreases insulin resistance and lowers inflammatory cytokines in aging humans. Aging, 3 (5), 533–542.
Bao, A.-M., Meynen, G., Swaab, D. F. (2008). The stress system in depression and neurodegeneration: Focus on the human hypothalamus. Brain Research Reviews, 57 (2), 531–553. doi: 10.1016/j.brainresrev.2007.04.005
McNelis, J. C., Manolopoulos, K. N., Gathercole, L. L., Bujalska, I. J., Stewart, P. M., Tomlinson, J. W., Arlt, W. (2013). Dehydroepiandrosterone exerts antiglucocorticoid action on human preadipocyte proliferation, differentiation, and glucose uptake. AJP: Endocrinology and Metabolism, 305 (9), E1134–E1144. doi: 10.1152/ajpendo.00314.2012
Ohlsson, C., Labrie, F., Barrett-Connor, E., Karlsson, M. K., Ljunggren, Ö., Vandenput, L. et. al (2010). Low Serum Levels of Dehydroepiandrosterone Sulfate Predict All-Cause and Cardiovascular Mortality in Elderly Swedish Men. The Journal of Clinical Endocrinology & Metabolism, 95 (9), 4406–4414. doi: 10.1210/jc.2010-0760
Barrett-Connor, E., von Mühlen, D., Laughlin, G. A., Kripke, A. (1999). Endogenous Levels of Dehydroepiandrosterone Sulfate, but Not Other Sex Hormones, Are Associated with Depressed Mood in Older Women: The Rancho Bernardo Study. Journal of the American Geriatrics Society, 47 (6), 685–691. doi: 10.1111/j.1532-5415.1999.tb01590.x
Fukui, M., Kitagawa, Y., Ose, H., Hasegawa, G., Yoshikawa, T., Nakamura, N. (2007). Role of Endogenous Androgen Against Insulin Resistance and Athero-sclerosis in Men with Type 2 Diabetes. Current Diabetes Reviews, 3 (1), 25–31. doi: 10.2174/157339907779802094
Amato, M. C., Giordano, C., Galia, M., Criscimanna, A., Vitabile, S., Midiri, M., Galluzzo, A. (2010). Visceral Adiposity Index: A reliable indicator of visceral fat function associated with cardiometabolic risk. Diabetes Care, 33 (4), 920–922. doi: 10.2337/dc09-1825
Petta, S., Amato, M., Cabibi, D., Cammà, C., Di Marco, V., Giordano, C. et. al (2010). Visceral adiposity index is associated with histological findings and high viral load in patients with chronic hepatitis C due to genotype 1. Hepatology, 52 (5), 1543–1552. doi: 10.1002/hep.23859
Andrews, R. C., Herlihy, O., Livingstone, D. E. W., Andrew, R., Walker, B. R. (2002). Abnormal Cortisol Metabolism and Tissue Sensitivity to Cortisol in Patients with Glucose Intolerance. The Journal of Clinical Endocrinology & Metabolism, 87 (12), 5587–5593. doi: 10.1210/jc.2002-020048
Apostolova, G. (2004). Dehydroepiandrosterone inhibits the amplification of glucocorticoid action in adipose tissue. AJP: Endocrinology and Metabolism, 288 (5), E957–E964. doi: 10.1152/ajpendo.00442.2004
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