Resting metabolic rate in obese diabetic and obese non-diabetic subjects and its relation to glycaemic control

Azza O Alawad, Tarig H Merghani, Mansour A Ballal, Azza O Alawad, Tarig H Merghani, Mansour A Ballal

Abstract

Background: Both obesity and type II diabetes mellitus are associated with insulin resistance and abnormal metabolic reactions. This study was conducted to evaluate resting metabolic rate in obese diabetic patients and to assess its relation to glycaemic control.

Results: This is a case control study conducted in Gabir AbuEliz centre in Khartoum, Sudan. A random sample of 40 obese diabetic patients (cases) and 40 obese non-diabetic subjects (controls) were interviewed and examined clinically to exclude presence of acute or chronic medical illness. Haemoglobin A1c was measured for each participant using the "NycoCard Haemoglobin A1c test" (Axis -Shield/ Norway). Fasting blood sugar was measured using one touch(R) glucometer (LifeScan Canada Ltd). The PowerLab 8/35 with a gas analyzer (AD Instruments, Castle Hill Australia) was used for measurement of VO2, VCO2 and Respiratory exchange ratio (RER). Resting metabolic rate was calculated using the Weir equation. VO2 (mean+/-SD) ml/min was significantly higher among cases (209.9+/-42.7) compared to the controls (192.4+/-28.1), (P = 0.034). Similarly, VCO2 (mean+/-SD) ml/min was higher among cases (191.4+/-35.0) than controls (178.3+/-22.5), (P = 0.05). Resting metabolic rate "RMR" (mean+/-SD) kcal/day was higher in obese diabetic patients (1480.7 +/- 274.2) than obese non-diabetic subjects (1362.4+/- 184.8), (P = 0.027). Participants with high glycated haemoglobin had higher RMR than those with normal glycated haemoglobin (P = 0.016).

Conclusion: It is concluded that resting metabolic rate is significantly higher in obese diabetic patients compared to obese non-diabetics, especially in those with poor glycaemic control.

References

    1. de Weir JB. New methods for calculating metabolic rate with special reference to protein metabolism. J Physiol. 1949;109:1–9.
    1. Mansell PI, Macdonald IA. Reappraisal of the Weir equation for calculation of metabolic rate. AJP - Regu Physiol. 1990;258(6):R1347–R1354.
    1. American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care. 2010;33(Suppl 1):S62–S69.
    1. Weyer C, Bogardus C, Pratley RE. Metabolic factors contributing to increased resting metabolic rate and decreased insulin-induced thermogenesis during the development of type 2 diabetes. Diabetes. 1999;48:1607–1614. doi: 10.2337/diabetes.48.8.1607.
    1. Fontvieille AM, Lillioja S, Ferraro RT, Schulz LO, Rising R, Ravussin E. Twenty-four-hour energy expenditure in Pima Indians with type 2 (non-insulindependent) diabetes mellitus. Diabetologia. 1992;35:753–759.
    1. Huang KC, Kormas N, Steinbeck K, Loughnan G, Caterson ID. Resting metabolic rate in severely obese diabetic and nondiabetic subjects. Obesity research. 2004;53(11):1395–1398.
    1. Martin K, Wallace P, Rust PF, Gravey WT. Estimation of resting energy expenditure considering effects of race and diabetes status. Diabetes Care. 2004;27:1405–1411. doi: 10.2337/diacare.27.6.1405.
    1. Henry CJK, Rees DG. New predictive equations for the estimation of basal metabolic rate in tropical people. Eur J Clin Nutr. 1991;45:177–185.
    1. World Medical Association Medical Ethics Committee. Updating the WMA declaration of Helsinki. Wld Med J. 1999;45:11–13.
    1. Felig P, Wahren J, Hendler R. Influence of maturity-onset diabetes on splanchnic glucose balance after oral glucose ingestion. Diabetes. 1978;27:121–126. doi: 10.2337/diab.27.2.121.
    1. Franssila-Kallunki A, Groop L. Factors associated with basal metabolic rate in patients with type 2 (non-insulin-dependent) diabetes mellitus. Diabetologia. 1992;35:962–966. doi: 10.1007/BF00401426.
    1. Gougeon R, Pencharz PB, Marliss EB. Effect of NIDDM on the kinetics of whole-body protein metabolism. Diabetes. 1994;43:318–328. doi: 10.2337/diab.43.2.318.
    1. Huggett RJ, Scott EM, Gilbey SG, Stoker JB, Mackintosh AF, Mary DA. Impact of type 2 diabetes mellitus on sympathetic neural mechanisms in hypertension. Circulation. 2003;108:3097–3101. doi: 10.1161/01.CIR.0000103123.66264.FE.
    1. Charlton MR, Nair KS. Role of hyperglucagonemia in catabolism associated with type 1 diabetes: effects on leucine metabolism and the resting metabolic rate. Diabetes. 1998;47(11):1748–1756. doi: 10.2337/diabetes.47.11.1748.
    1. Nair S, Halliday D, Garrow J. Increased energy expenditure in poorly controlled type 1 insulin-dependent diabetic patients. Diabetologia. 1984;27:13–16.
    1. Cryer PE. Minireview: Glucagon in the pathogenesis of hypoglycemia and hyperglycemia in diabetes. Endocrinology. 2012;153(3):1039–1048. doi: 10.1210/en.2011-1499.
    1. Johnstone AM, Murison SD, Duncan JS, Rance KA, Speakman JR, Koh YO. Factors influencing variation in basal metabolic rate include fat-free mass, fat mass, age, and circulating thyroxine but not sex, circulating leptin, or triiodothyronine. Am J Clin Nutr. 2005;82(5):941–948.
    1. Adriaens MP, Schoffelen PF, Westerterp KR. Intra-individual variation of basal metabolic rate and the influence of daily habitual physical activity before testing. Br J Nutr. 2003;90(2):419–423. doi: 10.1079/BJN2003895.
    1. Elbagir MN, Eltom MA, Rosling H, Berne C. Glycaemic control of insulin-dependent diabetes mellitus in Sudan: influence of insulin shortage. Diabetes Res Clin Pract. 1995;30(1):43–52. doi: 10.1016/0168-8227(95)01145-5.

Source: PubMed

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