Dietary cassava, β-cell function and hyperbolic product loss rate in type 2 diabetes patients from South Kivu

Abstract

Objective Cassava, a major carbohydrate source in Africa, contains potentially diabetogenic chemicals, although its consumption is not associated with incident diabetes. As it is not known whether cassava intake impairs residual β-cell function in patients with type 2 diabetes (T2D), our study compared the metabolic phenotypes of diet- and/or oral antidiabetic drug (OAD)-treated T2D patients in South Kivu (Democratic Republic of the Congo) with [Cassava (+); n = 147] and without [Cassava (–); n = 46] self-reported cassava consumption. Design & methods A total of 193 patients [male:female (%) 37:63; mean ± 1 SD age: 56 ± 11 years] were interviewed to determine the frequency and distribution of eight major dietary carbohydrate (CHO) sources (cassava, plantain, rice, maize, bread, sorghum, potatoes and legumes). Fasting glucose, insulin and lipid levels were obtained after an overnight fast and OAD discontinuation. Cassava (+) and Cassava (–) groups were compared for HOMA indices of insulin sensitivity (S), beta-cell function (B), hyperbolic product (B × S) and B × S loss rate (B × S LR). Results Diabetes duration was 6 ± 7 years, age at diabetes diagnosis was 51 ± 11 years and BMI was 25 ± 5 kg/m 2. Cassava intake was reported by 76% of patients, and amounted to 29 ± 11% of their daily CHO intake. The Cassava (–) group ate more plantain, maize, bread and potatoes, and less sorghum. Age, gender and age at diabetes diagnosis did not differ between Cassava (+) and (–) patients, nor did BMI, fat mass, waist circumference, lipid profile and metabolic syndrome prevalence. HOMA indices of S, B, B × S and B × S LR did not differ significantly between groups-Cassava (+) vs (–): S, 114 ± 56% vs 114 ± 60%; B, 34 ± 30% vs 39 ± 32%; B × S, 38 ± 35% vs 40 ± 31%; and B × S LR, 1.19 ± 0.84% vs 1.09 ± 0.65% per year-nor did the glucose-lowering modalities. Conclusion Cassava consumption in South Kivu is not associated with changes in T2D phenotype or in the glucose homoeostasis determinants S, B, B × S and B × S LR. Cassava consumption does not accelerate β-cell function loss in such a population, whose markedly compromised glucose homoeostasis renders them vulnerable to environmentally acquired β-cell impairment.