Treated Type 2 Diabetes Patients Research Articles

Effect of Cucurbita ficifolia Bouché on glutathione level and glycosylated hemoglobin percentage in a Mexican rural population with type 2 diabetes

Ethnopharmacological importanceCucurbita ficifolia Bouché fruit is widely used in Mexican traditional medicine to treat type 2 diabetes (T2D) because it has been attributed with antioxidant and hypoglycemic properties in different experimental models and T2D patients. An imbalance in physiological glutathione (GSH) concentrations increases the susceptibility to developing complications associated with oxidative stress in T2D patients. Aim of the studyTo investigate the effect of C. ficifolia on the antioxidant properties of GSH, general health measurements, and biochemical parameters in a Mexican rural population, and to evaluate the changes in socio-affective scores of patients due to improvement in T2D. Materials and methodsTwenty-seven women diagnosed with T2D with poor glycemic control volunteered and were divided into two groups: C. ficifolia (0.5 g/kg of fresh pulp weight) with hypoglycemic pharmacotherapy, and another group with only hypoglycemic pharmacotherapy, for 12 weeks. We evaluated the effect of the fresh pulp of C. ficifolia on body mass index, blood pressure, glucose, glycosylated hemoglobin, cholesterol, triglycerides, and GSH. Expanding the study, we evaluated the quality of life, anxiety, and depression scores before and after the intervention. ResultsTreatment with the fresh pulp of C. ficifolia for 12 weeks reduced glycosylated hemoglobin, similar to the hypoglycemic pharmacotherapy group, and significantly increased GSH concentrations. The patients' moods did not change despite increased GSH concentrations and improved T2D control. ConclusionsThe increased GSH concentrations due to the consumption of fresh pulp of C. ficifolia could help to protect against oxidative stress and extend therapeutic benefits in addition to the usual hypoglycemic drugs in patients with T2D.

Use of gliptins reduces levels of SDF-1/CXCL12 in bullous pemphigoid and type 2 diabetes, but does not increase autoantibodies against BP180 in diabetic patients.

The use of dipeptidyl peptidase 4 (DPP4) inhibitors, (also known as gliptins), is associated with an increased risk of bullous pemphigoid (BP), an autoimmune blistering skin disease. To explore the mechanism behind gliptin-associated BP we investigated circulating autoantibodies against the major BP autoantigen BP180 in serum samples from patients with type 2 diabetes (T2D) with preceding gliptin medication (n = 136) or without (n = 136). Sitagliptin was the most frequently prescribed gliptin (125/136 patients). Using an ELISA assay, we showed that IgG autoantibodies against the immunodominant NC16A domain of BP180 were found in 5.9% of gliptin treated and in 6.6% of non-gliptin treated T2D patients. We found that 28% of gliptin treated patients had IgG autoantibodies recognizing the native full-length BP180 in ELISA, but among non-gliptin treated the seropositivity was even higher, at 32%. Further ELISA analysis of additional serum samples (n = 57) found no major changes in the seropositivity against BP180 during a follow-up period of about nine years. In immunoblotting, full-length BP180 was recognized by 71% of gliptin treated and 89% of non-gliptin treated T2D patients, but only by 46% of the age-and sex-matched controls. The chemokine stromal derived factor-1(SDF-1/CXCL12) is one of the major substrates of DPP4. Immunostainings showed that the expression of SDF-1 was markedly increased in the skin of BP patients, but not affected by prior gliptin treatment. We found that the use of gliptins decreased the serum level of SDF-1α in both BP and T2D patients. Our results indicate that the autoantibodies against the linear full-length BP180 are common in patients with T2D, but seropositivity is unaffected by the use of sitagliptin.

Metformin does not prevent the alteration of reticulum-mitochondria Ca2+ coupling and the progression towards early diabetic cardiomyopathy with HFpEF in a diet-induced mouse model of T2D

Diabetic cardiomyopathy, as a major complication of type 2 diabetes (T2D), shows a rising prevalence nowadays. Reticulum-mitochondria Ca2+ uncoupling was recently reported as an early but reversible trigger of cardiac dysfunction using a diet-induced murine model of DCM with heart failure and preserved ejection fraction (HFpEF). Metformin is the first-line treatment prescribed to treat T2D patients, with known protective effects against myocardial infarction. We here aimed to determine if metformin could hinder the alteration of the reticulum-mitochondria Ca2+ coupling and the cardiac dysfunction induced by a high-fat high-sucrose diet (HFHSD) in mice. Mice were either fed a HFHSD or a standard diet for 16 weeks. During the last 6 weeks of diet, HFHSD mice received a daily oral gavage with either metformin or vehicle. Reticulum-mitochondria Ca2+ coupling was assessed: 1) structrally by proximity ligation assay between IP3R and VDAC; and 2) functionally by Ca2+ imaging of the mitochondrial Ca2+ sensor, 4mtD3cpv, expressed by intramyocardial adenoviral injection. Echocardiography was perfomed on lightly anesthetized animals to assess systolic function and hypertrophy. Metformin rescued the glucose tolerance and insulinemia in HFHSD mice, but partially for the cardiac insulin resistance. However, in the HFHSD cardiomyocyte, metformin did not preclude the reduction of the proximity between IP3R and VDAC, and of the histamine-driven reticulum-mitochondria Ca2+ transfer through the IP3R-VDAC complex. Echocardiography also revealed no prevention of HFHSD-induced cardiac hypertrophy and strain rate reduction. Our data report that 6 weeks of metformin treatment did not preserve the reticulum-mitochondria Ca2+ coupling in the diabetic heart and did not prevent the progression towards early DCM with HFpEF.

Observational study on dietary changes of participants following a multicomponent lifestyle program (Reverse Diabetes2 Now).

Lifestyle intervention studies to treat type 2 diabetes (T2D) are on the rise. However, in-depth research is lacking into the dietary changes that participants make. The present study aimed to observe the dietary intake of participants following the group program 'Reverse Diabetes2 Now' (RD2N) over 12 months. The web-based 24-h dietary recall-tool Compl-eat was used to collect dietary intake data. In total, 147 T2D patients were included in a cross-sectional study (n = 37 at baseline, n = 58 at 6 months, n = 52 at 12 months). A lower intake of total energy, carbohydrates and iodine was found for the groups at 6 and 12 months compared to the baseline group. The absolute consumption of total fat and saturated fat did not differ between the groups; only the percentage as total calorie consumption decreased. Consumption of vegetables and full-fat yoghurt was higher in groups at 6 and 12 months compared to the group at baseline. Consumption of bread, cakes and sweet biscuits, pasta/rice/tortillas, artificially sweetened soft drinks, and crisps were lower in the groups at 6 and 12 months compared to the group at baseline. Similar results were observed in a separate prospective study in 22 participants over 12 months following the same lifestyle-intervention. Overall, participants shifted their dietary intake somewhat towards a healthier dietary pattern with overall lower energy and carbohydrates and more vegetables. Moreover, participants largely maintained this healthier pattern over 12 months. There were some concerns regarding iodine intake. These promising results need to be confirmed in a fully-scaled study, as well in a comparison with controls.

Fasting in diabetes treatment (FIT) trial: study protocol for a randomised, controlled, assessor-blinded intervention trial on the effects of intermittent use of a fasting-mimicking diet in patients with type 2 diabetes

BackgroundCaloric restriction is an effective way to treat Type 2 diabetes (T2D). However, chronic and severe restriction of food intake is difficult to sustain and is known to promote slower metabolism. Intermittent and frequent fasting can exert similar metabolic effects, but may be even more challenging for most patients. A fasting-mimicking diet (FMD) is low in calories, sugars and proteins, but includes relatively high levels of plant based complex carbohydrates and healthy fats. The metabolic effects of such a diet mimic the benefits of water-only fasting. The effects of a FMD applied periodically in T2D patients are still unknown. The Fasting In diabetes Treatment (FIT) trial was designed to determine the effect of intermittent use (5 consecutive days a month during a year) of a FMD in T2D patients on metabolic parameters and T2D medication use compared to usual care.MethodsOne hundred T2D patients from general practices in the Netherlands with a BMI ≥ 27 kg/m2, treated with lifestyle advice only or lifestyle advice plus metformin, will be randomised to receive the FMD plus usual care or usual care only. Primary outcomes are HbA1c and T2D medication dosage. Secondary outcomes are anthropometrics, blood pressure, plasma lipid profiles, quality of life, treatment satisfaction, metabolomics, microbiome composition, MRI data including cardiac function, fat distribution and ectopic fat storage, cost-effectiveness, and feasibility in clinical practice.DiscussionThis study will establish whether monthly 5-day cycles of a FMD during a year improve metabolic parameters and/or reduce the need for medication in T2D. Furthermore, additional health benefits and the feasibility in clinical practice will be measured and a cost-effectiveness evaluation will be performed.Trial registrationThe trial was registered on ClinicalTrials.gov. Identifier: NCT03811587. Registered 21th of January, 2019; retrospectively registered.

1158-P: Type 2 Diabetes Patients Subtype Analysis: Unbiased Machine Learning for Future Personalized T2D Care

Dorzagliatin (HMS5552) that achieved POC in a recent Ph II trial, demonstrated its potential to treat type 2 diabetes (T2D) patients through a personalized medicine approach in a biomarker guided patient selection study. We here by conducted a data-driven unsupervised clustering analysis on the full analysis set (221 patients) of Dorzagliatin Ph II trail using clinically relevant biomarkers, which generated six clusters. An ANOVA test was done for those variables between clusters, and 40 of them are significantly different (P < 0.05). The study showed that each cluster possesses unique characters related to disease stage of T2D and the stage is progressing to one direction which starts from mild to severe loss of pancreas β-cell function accompany with progressively increase of insulin resistance. Cluster 1 shared similar feature as those in previous Ph Ic study, in which, QD dose of Dorzagliatin offered better response rate of 100%, while in Ph II based cluster, the 75mg QD dose group achieved 1.88% reduction in HbA1c from baseline with the 75mg BID offered HbA1c reduction of 0.95%. However, in Cluster 2 and 4, there are clear trends that BID is more effective than QD in glycemic control as well as improving β-cell function and reduction of insulin resistance. In Cluster 4, it is observed FPG reduction of 1.57mmol/L, PPG reduced of 2.73mmol/L, HOMA-β improvement of 12.22, and HbA1c reduction of 1.69% in 75mg BID dose group, with corresponding changes in 75 QD group of 0.35 mmol/L, 1.7mmol/L, 9.24 and 0.26% respectively adjusted by placebo. The results suggested that the AI methodology is able to differentiate T2D patients into different subclass according to the severity of the disease state, and 75mg BID Dorzagliatin seems offered a minimum therapeutic effective dose (MTED) to all patient population, and 75mg QD regiment is a preferred option for the early stage T2D condition. Disclosure L. Chen: Employee; Self; Hua Medicine. L. Feng: Employee; Self; Hua Medicine. C. Tang: Employee; Self; Hua Medicine. Y. Zhang: Employee; Self; Hua Medicine. Funding Hua Medicine

1156-P: Duodenal Mucosal Resurfacing (DMR) Combined with GLP-1 RA May Eliminate Insulin Therapy and Improve Metabolic Health in Type 2 Diabetes

Background: Duodenal mucosal resurfacing (DMR) is an endoscopic intervention in which the duodenal mucosa is ablated by hydrothermal energy. DMR improves glycemic control in type 2 diabetes (T2D) through altered metabolic signaling from the duodenum causing insulin sensitization. We studied the feasibility of eliminating insulin therapy in T2D by combining DMR with GLP-1r agonism (liraglutide) and lifestyle counseling. Methods: Single arm, single center study in 16 insulin treated T2D patients (HbA1c ≤64 mmol/mol; basal insulin <1U/kg/day, c-peptide ≥0.5 nmol/l). Day 1, DMR is administered and insulin therapy discontinued. Day 14, liraglutide is introduced (titrated to 1.8 mg/day) and life style counseling is administered throughout. Primary endpoint: percentage of patients free of insulin and HbA1c ≤59 mmol/mol at 6 months. Results: Enrolment has been completed and 9 patients have reached 6 months with 8/9 (89%) insulin-free and able to maintain glycemic control with improvement across multiple metabolic parameters (Table 1). Conclusion: Single endoscopic DMR, combined with liraglutide and lifestyle counseling, may effectively eliminate the need for insulin therapy in T2D while improving overall metabolic health. This treatment approach is a promising alternative that appears to shift insulin-treated T2D patients to a state of better overall metabolic health. Disclosure P. Smeele: None. A.C. van Baar: None. T.M. Vriend: None. F. Holleman: Advisory Panel; Self; AstraZeneca, Boehringer Ingelheim International GmbH, Sanofi. M. Soeters: None. M. Nieuwdorp: Advisory Panel; Self; Caelus health. J. Tijssen: None. J.J. Bergman: Research Support; Self; Fractyl Laboratories, Inc.

Metformin increases glucose uptake and acts renoprotectively by reducing SHIP2 activity.

Metformin, the first-line drug to treat type 2 diabetes (T2D), inhibits mitochondrial glycerolphosphate dehydrogenase in the liver to suppress gluconeogenesis. However, the direct target and the underlying mechanisms by which metformin increases glucose uptake in peripheral tissues remain uncharacterized. Lipid phosphatase Src homology 2 domain-containing inositol-5-phosphatase 2 (SHIP2) is upregulated in diabetic rodent models and suppresses insulin signaling by reducing Akt activation, leading to insulin resistance and diminished glucose uptake. Here, we demonstrate that metformin directly binds to and reduces the catalytic activity of the recombinant SHIP2 phosphatase domain in vitro. Metformin inhibits SHIP2 in cultured cells and in skeletal muscle and kidney of db/db mice. In SHIP2-overexpressing myotubes, metformin ameliorates reduced glucose uptake by slowing down glucose transporter 4 endocytosis. SHIP2 overexpression reduces Akt activity and enhances podocyte apoptosis, and both are restored to normal levels by metformin. SHIP2 activity is elevated in glomeruli of patients with T2D receiving nonmetformin medication, but not in patients receiving metformin, compared with people without diabetes. Furthermore, podocyte loss in kidneys of metformin-treated T2D patients is reduced compared with patients receiving nonmetformin medication. Our data unravel a novel molecular mechanism by which metformin enhances glucose uptake and acts renoprotectively by reducing SHIP2 activity.—Polianskyte-Prause, Z., Tolvanen, T. A., Lindfors, S., Dumont, V., Van, M., Wang, H., Dash, S. N., Berg, M., Naams, J.-B., Hautala, L. C., Nisen, H., Mirtti, T., Groop, P.-H., Wähälä, K., Tienari, J., Lehtonen, S. Metformin increases glucose uptake and acts renoprotectively by reducing SHIP2 activity.

Early Changes in Glucose Homeostasis after Gastric Bypass Surgery in Patients with T2DM—Role of Adipose Tissue Mechanisms?

Gastric bypass (GBP) surgery can effectively prevent or treat type 2 diabetes (T2D). Adipose tissue (AT) mechanisms may be important, but causality is not shown. We studied the relationship between early changes in whole-body and AT metabolism in obese T2D patients. Methods: Eight T2D patients with BMI 30-45 (M/F 3/5, age 49 ± 10) underwent GBP following 4 week low calorie diet. Assessments: OGTT, AT biopsies to measure gene expression in AT and in adipocytes size, glucose uptake (GU), lipolysis and insulin action. Results: At 4 and 24 weeks post-GBP, all subjects but one stopped diabetes medication. The Matsuda index increased compared to baseline, while HOMA-IR, fasting glucose, HbA1c and insulin levels decreased (p <0.01 for all). In adipocytes, basal, isoprenaline-stimulated or insulin-inhibited lipolysis rates and basal or insulin-stimulated GU did not change significantly. Mean adipocyte size was reduced, more at 4 than 24 weeks. At 4 week, expression of genes involved in fatty acid oxidation, CPT1b; cell proliferation, E2F1; and adiponectin were increased, whereas leptin was reduced (p<0.for all). Conclusion: Glycemic control and insulin sensitivity clearly improved 4 weeks after GBP, but adipocyte insulin sensitivity in vitro did not improve despite a reduction in adipocyte size. Thus the mechanisms for rapid improvement of T2D after GBP may occur mainly in other tissues than adipose.Clinical and metabolic characteristicsBaseline4-wks post surgery24-wks post surgeryAdipocyte in-vitro dataBaseline4-wks post surgery24-wks post surgeryBMI (kg/m2)37.3 ± 4A32.9 ± 3.3B28.3 ± 3.5CAdipocyte diameter (µm)110 ± 5.3A72.3 ± 10.3B92.5 ± 5.4CWeight (kg)105.5 ±14.5A93.4 ± 11.4B80.1 ± 11.1CGlucose uptake (fL/cell/sec)Waist hip ratio (cm)0.99 ± 0.07a0.97 ± 0.07a0.93 ± 0.07bbasal19.5 ± 4.316.6 ± 6.720.3 ± 3.8Body fat (%)41.2 ± 8.9A38.6 ± 8.9B30.7 ± 10.4C25 µU/ml Insulin23.1 ± 6.319.2 ± 7.629.8 ± 6.7HbA1c (mmol/mol)48 ± 6a39 ± 7b37 ± 4b1000 µU/ml Insulin31.4 ± 4.725.7 ± 10.739.4 ± 6.9Fasting glucose (mmol/L)7.4 ± 0.9A5.8 ± 0.6B5.4 ± 04CLipolysis (nmol gly-cerol/10E5 cells/h)HOMA-IR6.63 ± 0.5A2.59 ± 1.3B1.32 ± 0.5C0.5 µM Iso58.4 ± 16.253.2 ± 9.351.3 ± 12.9Matsuda index1.38 ± 0.3A2.77 ± 0.9B4.90 ± 2.1C0.5 µM Iso + 1µU/ml insulin33.1 ± 6.527.3 ± 6.941.7 ± 10.7Modified QUICKI0.29 ± 0.01A0.33 ± 0.3B0.38 ± 0.03C0.5 µM Iso + 100 µU/ml insulin26.4 ± 4.321.6 ± 5.433.1 ± 9.1Data are means ± SD. Body fat % measured by bioimpedance. Different letters indicated significant differences between the visits; lower case letter: p < 0,; upper case letter: p < 0,01. Iso, isoprenaline. Disclosure P. Katsogiannos: None. G.J. Boersma: None. P.G. Kamble: None. M.J. Pereira: None. P. Lundkvist: None. A. Karlsson: None. M. Sundbom: None. J.W. Eriksson: Employee; Spouse/Partner; Amgen Inc.. Consultant; Self; AstraZeneca. Research Support; Self; AstraZeneca. Consultant; Self; Novo Nordisk A/S, Merck Sharp & Dohme Corp.. Research Support; Self; Bristol-Myers Squibb Company.

Interaction of rs316019 variants of SLC22A2 with metformin and other drugs- an in silico analysis.

Metformin is one of the first-line and most widely prescribed drugs to treat type 2 diabetes (T2D). Its clearance from circulation is mostly facilitated by SLC22A2 (OCT2) in the renal cells. SLC22A2 is a polyspecific organic cation transporter and mediate transport of structurally unrelated endogenous and exogenous compounds including many drugs. rs316019 (p.270A > S) is the most common variant of SLC22A2 with a frequency as high as 15% or more in many populations. The 270S form of SLC22A2 clears metformin from circulation at much reduced level compared to the 270A form. If accumulated, metformin increases plasma lactate level in a concentration-dependent manner which can lead to a condition known as metformin-associated lactic acidosis (MALA). MALA is a potentially life-threatening complication with a mortality rate of 30–50%. Pre-existing clinical conditions, such as renal impairment, sepsis, anoxia, etc may make individuals more prone to MALA. In this study, we used computational approaches to investigate the effect of 270A > S change in SLC22A2 on interaction with metformin and other drugs. Based on the structural models, all substrates bind to the same pocket of SLC22A2. The substrates fit better to the binding site of 270A form of SLC22A2. The binding site has a few core interacting residues, among which SER358 appears to be the most important. It is an in silico prediction that the T2D patients, who are under metformin regimen, should be cautious in taking ranitidine (an over-the-counter sold drug) on a regular basis as it may lead to metformin associated lactate accumulation in blood.

Demographic and clinical profiles of type 2 diabetes mellitus patients initiating sitagliptin in the real-world setting

Objective: Dipeptidyl peptidase-4 (DPP-4) inhibitors have been used for the management of type 2 diabetes (T2D) for over a decade; however, there is a limited understanding of the evolution of their use in the real-world setting over this time period. This study evaluated the demographics and clinical characteristics of patients initiating sitagliptin over a 10 year period in the United States.Research design and methods: Quintiles electronic medical records database was used to identify adults with a new prescription of sitagliptin over two 5 year time periods: 2006–2010 (n = 57,604), and 2011–2015 (n = 147,326). In addition, we also evaluated how the most recent (year 2015) profile of sitagliptin initiators (n = 29,295) compares to the treated T2D patients (N = 474,877) in 2015.Main outcome measures: No outcomes were assessed. Descriptive statistics were used to summarize baseline patient characteristics.Results: The overall demographics and clinical characteristics of patients initiating sitagliptin were generally similar over the two time periods; however, baseline HbA1c (median) was higher in the later time period: 7.6% vs. 7.9% respectively. Sitagliptin was initiated in patients across a broad range of age (18–79) years, body mass index (BMI) (10–70) kg/m2 and HbA1c (3–20) %. The most prevalent comorbidities observed in these patients were hypertension (93%), hyperlipidemia (81%), obesity (55%), chronic kidney disease (22%) and cardiovascular disease (21%). Additionally, when we assessed the treated T2D patients and patients initiating sitagliptin in 2015, several characteristics were comparable such as age (median) (64 vs. 63) years and BMI (33 vs. 33) kg/m2, and the most prevalent comorbidities were hypertension (97 vs. 95) %, and hyperlipidemia (86 vs. 81) % respectively.Conclusion: The overall demographic and comorbidity profile of patients initiating sitagliptin did not substantially change over the last decade and is similar to the treated T2D population.

Evaluation of IGFBP-7 DNA methylation changes and serum protein variation in Swedish subjects with and without type 2 diabetes

BackgroundInsulin-like growth factor-binding protein 7 (IGFBP-7) is able to interact with insulin-like growth factor 1 (IGF-1) as well as insulin. Previous studies have suggested that serum IGFBP-7 levels may be associated with insulin resistance in type 2 diabetes (T2D). This study aimed to evaluate IGFBP-7 serum protein and IGFBP7 DNA methylation levels in the subjects with and without T2D.ResultsA total of 340 Swedish subjects including 100 newly diagnosed T2D patients (50 women/50 men), 100 age-matched nondiabetic control subjects (50/50) and 140 treated T2D patients (54/86) were studied. Serum IGFBP-7 levels were measured with a novel ELISA. IGF1, IGFBP-1, and insulin were determined by in-house radioimmunoassays. DNA methylation levels in the IGFBP7 gene were analyzed with a bisulfite-pyrosequencing technique. Serum IGFBP-7 protein levels were similar among nondiabetic subjects, newly diagnosed, and treated T2D patients and were not correlated with IGFBP7 DNA methylation. However, IGFBP7 DNA methylation was increased in men with newly diagnosed T2D compared with nondiabetic controls (17.6% vs. 12.5%, P < 0.01). Serum IGFBP-7 levels correlated (r = 0.331, P = 0.019) with serum IGFBP-1 levels, a marker of insulin production, in men but not women with newly diagnosed T2D.ConclusionsThis study demonstrates for the first time that IGFBP7 DNA methylation levels are increased in Swedish men with newly diagnosed T2D. The correlation between IGFBP-7 and IGFBP-1 suggests that low IGFBP-7 may be associated with insulin resistance in T2D.

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

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.