ISSN No. 1606-7754                   Vol.13 No.1  April 2005

Insulin resistance in type 2 diabetic Nigerians.
Adamu G Bakari and Geoffrey C Onyemelukwe
Department of Medicine, Ahmadu Bello University and Ahmadu Bello University Teaching Hospital Zaria, Nigeria


Considerable interest has been generated and still continues on the role of insulin resistance in the aetiology of glucose intolerance and its complications. There is evidence to suggest that racial factors are important in this regard. Whereas Caucasian studies suggest insulin resistance to be universal in type-2 diabetes, African-American studies on the other hand suggest the contrary in a significant proportion of type-2 diabetic African-Americans. No previous study has been undertaken in this aspect in type-2 diabetic Nigerians. Objective: To measure insulin resistance using the Homeostasis Model Assessment (HOMA) among type-2 diabetic Nigerians. Subjects and methods: A cross sectional study involving 40 type-2 diabetic subjects and 36 controls. The HOMA method was used to compute insulin resistance for each subject. Individual HOMA scores were subjected to statistical analysis between the two (diabetic and non-diabetic) groups. Results: Forty type 2 diabetic patients and 36 healthy age and socio-economic status matched control subjects were studied. Mean HOMA scores were significantly higher among type 2 diabetic subjects than controls. Ten (27.8%) of the control subjects demonstrated HOMA insulin resistance values greater than one compared to 35 (87.5%) of type-2 diabetic patients (p<0.05). Conclusion: It is concluded although type-2 diabetic patients exhibit more insulin resistance than control subjects, insulin sensitive variants of type-2 diabetes is also found in this population.

Key words: HOMA, Insulin resistance, type-2 diabetes, Nigerians


Type-2 diabetes mellitus is a heterogeneous disorder characterized by chronic hyperglycaemia due to dynamic interactions between varying defects of insulin secretion and insulin resistance. Either of these defects may be the predominant feature in a particular case.1

There is evidence to suggest that the underlying defect in type 2 diabetes varies from one population to another and even within populations. Martins et al2 established that insulin resistance precedes and strongly predicts the development of type 2 diabetes mellitus among whites in the United States, Banerji and Lebovitz3 on the other hand, noted that both insulin sensitive and insulin resistant forms of type 2 diabetes exist among African-American type 2 diabetic patients, with about 44 percent of such patients been insulin sensitive. More interestingly these observations were made even when type-2 diabetes was clinically manifest.

More recently, it has been shown that HOMA estimated insulin resistance is an independent predictor of cardiovascular disease in type-2 diabetic subjects.4

As opposed to the vast literature on insulin resistance among type 2 diabetic patients in technically advanced regions of the world, there is paucity of published material in Nigeria in particular and Africa in general. We report the first study on insulin resistance using the HOMA method in Nigerian type 2 diabetic patients.

Subjects and Methods

Type 2 diabetic patients attending the diabetic clinic of Ahmadu Bello University Teaching Hospital (ABUTH) Zaria, Nigeria, having ‘good’ glycaemic control, (defined as fasting blood sugar (FBS) of 4.4 to 6.7 mmol/l, and or a 2 hour post prandial blood sugar of 4.4 to 8.9 mmol/L) and ‘acceptable’ glycaemic control (FBS if 6.7 to 7.8 mmol/L and or 2 HPP of 8.9 to 10.0 mmol/L)5, on at least three clinic visits while on dietary therapy alone, or dietary therapy in addition to oral hypoglycaemic agent(s) formed the subjects of this study. Classification of patients as type 2 diabetics was however based on clinical grounds of non-dependence on insulin for survival.6 The exclusion criteria were insulin dependence, evidence of secondary diabetes, current insulin therapy or previous history of ketosis, and pregnancy. Use of oral contraceptives and clinical or biochemical evidence of disease of the liver, kidney or thyroid were also exclusion criteria.

Thirty-six healthy, age, sex and socio economic status matched volunteers who had no personal or family history of diabetes mellitus or hypertension were recruited to serve as controls. The exclusion criteria were clinical evidence of any illness, personal or family history of diabetes mellitus or hypertension, current use of any form of medication and engagement in competitive sport; factors known to interfere with insulin secretion and action.

Information on age, sex and anthropometric measures were obtained from all patients and control subjects. Weights (in Kg) were taken with only undergarments to the nearest 0.5 kg. Heights (in meters) were taken to the nearest 0.5 cm with subjects standing erect without shoes or headgear. Body Mass Index (BMI) was derived by dividing the weight by the square of the height.7

Metabolic studies

Oral hypoglycaemic agent therapy was withdrawn a week before metabolic studies to eliminate the effect of these drugs on insulin secretion.6

Following an overnight 10-12 hours fast, commencing between 21.00 to 22.00 hours the preceding night, 5mL of venous blood were drawn from each subject into EDTA treated tubes and promptly centrifuged. The plasma was then divided into aliquots for plasma glucose and insulin estimation. Aprotinin 200 KIU per ml of plasma8 was added to the aliquot for insulin assay; this was kept at -200Centigrade until analysis using a commercially available human insulin ELISA kit (DRG instruments Gmbh, Marburg, Germany, Cat no. EIA 2935). The kit has an inter-assay and intra-assay coefficients of variation of 5.2 % and 4.8% respectively, sensitivity of 99% for human insulin and no cross-reaction with pro-insulin. Plasma glucose analyses were done within an hour of collection of plasma using a glucose oxidase method. 9

Insulin resistance values were derived using the homeostasis model assessment (HOMA) method,10 employing the equation below.

Insulin resistance = (Fasting plasma insulin micro-units/L) X ( Fasting plasma Glucose mmol/L) 22.5

The figure 22.5 in the equation brings the insulin resistance value to 1.0 (insulin sensitivity of 100 %) of ‘normal’ subjects.

Results are presented as mean ± standard deviation. Unpaired student’s t-test was used to determine the differences between continuous variables while chi-square test was used for categorical variables. The level of statistical significance in each case was taken as p ≤ 0.05.

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