Insulin resistance and beta-cell function in different ethnic groups in Kenya: the role of abdominal fat distribution
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Little is known about the pathophysiology of diabetes in Africans. Thus, we assessed whether insulin resistance and beta-cell function differed by ethnicity in Kenya and whether differences were modified by abdominal fat distribution. A cross-sectional study in 1,087 rural Luo (n = 361), Kamba (n = 378), and Maasai (n = 348) was conducted. All participants had a standard 75-g oral glucose tolerance test (OGTT). Venous blood samples were collected at 0, 30, and 120 min. Serum insulin was analysed at 0 and 30 min. From the OGTT, we assessed the homoeostasis model assessment of insulin resistance by computer model, early phase insulin secretion, and disposition index (DI) dividing insulin secretion by insulin resistance. Abdominal subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) thickness were carried out by ultrasonography. Linear regression analyses were done to assess ethnic differences in insulin indices. The Maasai had 32 and 17 % higher insulin resistance than the Luo and Kamba, respectively (p < 0.001). Early phase insulin secretion was 16 % higher in the Maasai compared to the Luo (p < 0.001). DI was 12 % (p = 0.002) and 10 % (p = 0.015) lower in the Maasai compared to the Luo and Kamba, respectively. Adjustments of SAT (range 0.1–7.1 cm) and VAT (range 1.5–14.2 cm) largely explained these inter-group differences with the Maasai having the highest combined abdominal fat accumulation. The Maasai had the highest insulin resistance and secretion, but the lowest relative beta-cell function compared to the Luo and Kamba. These differences were primarily explained by abdominal fat distribution.
KeywordsInsulin resistance Insulin secretion Ethnicity Obesity
Homoeostasis model assessment of insulin resistance by computer model
Impaired fasting glucose
Impaired glucose tolerance
Oral glucose tolerance test
Abdominal subcutaneous adipose tissue
Visceral adipose tissue
We are grateful to all participants, the local chiefs and sub-chiefs, the local elder councils and district politicians. We are also indebted to the late Benedict Omondi (KEMRI), Tobias Oketch (CVBCR), Arthur J Ukumu (DVBD), Odero Sabiano (DVBD), and Saidi Kisiwa (KEMRI) for their skilful collection and analysis of blood samples in the field. Likewise, we sincerely thank all local assistants for their effort in excellent social mobilization and collection of data. We acknowledge the permission by the Director of KEMRI to publish this manuscript. The study was supported by DANIDA, Cluster of International Health (University of Copenhagen), Steno Diabetes Center, Beckett Foundation, Dagmar Marshall Foundation, Dr. Thorvald Madsen’s Grant, Kong Christian den Tiende’s Foundation, Brdr. Hartmann Foundation. The funding bodies had no role in the study design, data collection, data analysis, data interpretation or decision to publish the findings.
Conflict of interest
The authors declare no conflict of interest.
- 6.Amoah AG, Owusu SK, Ayittey OM, Schuster DP, Osei K (2001) Minimal model analyses of beta cell secretion, insulin sensitivity and glucose effectiveness in glucose tolerant, non-diabetic first-degree relatives of Ghanaian patients with type 2 diabetes and healthy control subjects. Ethn Dis 11:201–210PubMedGoogle Scholar
- 9.Jennings CL, Lambert EV, Collins M, Levitt NS, Goedecke JH (2009) The atypical presentation of the metabolic syndrome components in black African women: the relationship with insulin resistance and the influence of regional adipose tissue distribution. Metabolism 58:149–157PubMedCrossRefGoogle Scholar
- 17.WHO (1999) Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification of diabetes mellitus. World Health Organisation. WHO/NCD/NCS/99.2. (GENERIC), Geneva, pp 1–59Google Scholar
- 25.Faerch K, Vaag A, Holst JJ, Glumer C, Pedersen O, Borch-Johnsen K (2008) Impaired fasting glycaemia vs impaired glucose tolerance: similar impairment of pancreatic alpha and beta cell function but differential roles of incretin hormones and insulin action. Diabetologia 51:853–861PubMedCrossRefGoogle Scholar