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

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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.

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Most cited references 13

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Factors influencing variation in basal metabolic rate include fat-free mass, fat mass, age, and circulating thyroxine but not sex, circulating leptin, or triiodothyronine.

Alexandra Johnstone, Sandra Murison, Jackie S Duncan … (2005)

Basal metabolic rate (BMR) is the largest component of daily energy demand in Western societies. Previous studies indicated that BMR is highly variable, but the cause of this variation is disputed. All studies agree that variation in fat-free mass (FFM) plays a major role, but effects of fat mass (FM), age, sex, and the hormones leptin, triiodothyrionine (T3), and thyroxine (T4) remain uncertain. We partitioned the variance in BMR into within- and between-subject effects and explored the roles of FFM, FM, bone mineral content, sex, age, and circulating concentrations of plasma leptin, T3, and T4. This was a cross-sectional study of 150 white adults from northeast Scotland, United Kingdom. Only 2% of the observed variability in BMR was attributable to within-subject effects, of which 0.5% was analytic error. Of the remaining variance, which reflected between-subject effects, 63% was explained by FFM, 6% by FM, and 2% by age. The effects of sex and bone mineral content were not significant (P > 0.05). Twenty-six percent of the variance remained unexplained. This variation was not associated with concentrations of circulating leptin or T3. T4 was not significant in women but explained 25% of the residual variance in men. Our data confirm that both FFM and FM are significant contributors to BMR. When the effect of FM on BMR is removed, any association with leptin concentrations disappears, which suggests that previous links between circulating leptin concentrations and BMR occurred only because of inadequate control for the effects of FM.

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Impact of type 2 diabetes mellitus on sympathetic neural mechanisms in hypertension.

S Gilbey, F MacKintosh, David Mary … (2003)

Essential hypertension (EHT) is a major cardiovascular risk factor, and the additional presence of type 2 diabetes mellitus (DM2) increases this risk. However, although the sympathetic nerve hyperactivity of EHT is known to play a role in cardiovascular risk, the level of sympathetic nerve activity is known neither in DM2 nor in hypertensive type 2 diabetic patients (EHT+DM2). Therefore, we planned to quantify the vasoconstrictor sympathetic nerve activity in patients with EHT+DM2 and with DM2 relative to that in matched groups with EHT and normal blood pressure (NT). In 68 closely matched subjects with EHT+DM2 (n=17), DM2 (n=17), EHT (n=17), and NT (n=17), we measured resting muscle sympathetic nerve activity as the mean frequency of multiunit bursts (MSNA) and of single units (s-MSNA) with defined vasoconstrictor properties. The s-MSNA in EHT+DM2 (97+/-3.8 impulses/100 beats) was greater (at least P<0.001) than in EHT (69+/-3.4 impulses/100 beats) and DM2 (78+/-4.1 impulses/100 beats), and all these were significantly greater (at least P<0.01) than in NT (53+/-3.3 impulses/100 beats) despite similar age and body mass index. The MSNA followed a similar trend. In addition, the level of insulin was also raised in EHT+DM2 (20.4+/-3.6 microU/mL) and DM2 (18.1+/-3.1 microU/mL; at least P<0.05) compared with HT or NT. Patients with EHT+DM2, EHT, or DM2 had central sympathetic hyperactivity, although plasma insulin levels were raised only in EHT+DM2 and DM2. The combination of EHT and DM2 resulted in the greatest sympathetic hyperactivity and level of plasma insulin, and this hyperactivity could constitute a mechanism for the increased risks of this condition.

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Minireview: Glucagon in the pathogenesis of hypoglycemia and hyperglycemia in diabetes.

Philip Cryer (2012)

Pancreatic islet α-cell glucagon secretion is critically dependent on pancreatic islet β-cell insulin secretion. Normally, a decrease in the plasma glucose concentration causes a decrease in β-cell insulin secretion that signals an increase in α-cell glucagon secretion during hypoglycemia. In contrast, an increase in the plasma glucose concentration, among other stimuli, causes an increase in β-cell insulin secretion that signals a decrease, or at least no change, in α-cell glucagon secretion after a meal. In absolute endogenous insulin deficiency (i.e. in type 1 diabetes and in advanced type 2 diabetes), however, β-cell failure results in no decrease in β-cell insulin secretion and thus no increase in α-cell glucagon secretion during hypoglycemia and no increase in β-cell insulin secretion and thus an increase in α-cell glucagon secretion after a meal. In type 1 diabetes and advanced type 2 diabetes, the absence of an increment in glucagon secretion, in the setting of an absent decrement in insulin secretion and an attenuated increment in sympathoadrenal activity, in response to falling plasma glucose concentrations plays a key role in the pathogenesis of iatrogenic hypoglycemia. In addition, there is increasing evidence that, in the aggregate, suggests that relative hyperglucagonemia, in the setting of deficient insulin secretion, plays a role in the pathogenesis of hyperglycemia in diabetes. If so, abnormal glucagon secretion is involved in the pathogenesis of both hypoglycemia and hyperglycemia in diabetes.

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Author and article information

Contributors

Azza O Alawad

Tarig H Merghani

Mansour A Ballal

Journal

Journal ID (nlm-ta): BMC Res Notes

Journal ID (iso-abbrev): BMC Res Notes

Title: BMC Research Notes

Publisher: BioMed Central

ISSN (Electronic): 1756-0500

Publication date Collection: 2013

Publication date (Electronic): 26 September 2013

Volume: 6

Page: 382

Affiliations

[1 ]Department of Physiology, Faculty of Medicine, University of Al-Neelain, Khartoum, Sudan

[2 ]Department of Physiology, Faculty of Medicine, University of Tabuk, Tabuk, Saudi Arabia

[3 ]Department of Physiology, Faculty of Medicine, University of Science and Technology, Khartoum, Sudan

Article

Publisher ID: 1756-0500-6-382

DOI: 10.1186/1756-0500-6-382

PMC ID: 3850714

PubMed ID: 24070224

SO-VID: 6f375eb6-a012-43d2-835d-d9c952857b06

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 6 February 2013

Date accepted : 25 September 2013

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

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Abstract

Background

Results

Conclusion

Related collections

Research from Sudan

Most cited references 13

Factors influencing variation in basal metabolic rate include fat-free mass, fat mass, age, and circulating thyroxine but not sex, circulating leptin, or triiodothyronine.

Impact of type 2 diabetes mellitus on sympathetic neural mechanisms in hypertension.

Minireview: Glucagon in the pathogenesis of hypoglycemia and hyperglycemia in diabetes.

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Journal

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Article

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Cited by 17

Most referenced authors 330