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Individuals with type 2 diabetes (T2D) and dyslipidemia are at an increased risk of cardiovascular disease. Fibrates are a class of drugs prescribed to treat dyslipidemia, but variation in response has been observed. To evaluate common and rare genetic variants that impact lipid responses to fenofibrate in statin‐treated patients with T2D, we examined lipid changes in response to fenofibrate therapy using a genomewide association study (GWAS). Associations were followed‐up using gene expression studies in mice. Common variants in SMAD3 and IPO11 were marginally associated with lipid changes in black subjects (P < 5 × 10‐6). Rare variant and gene expression changes were assessed using a false discovery rate approach. AKR7A3 and HSD17B13 were associated with lipid changes in white subjects (q < 0.2). Mice fed fenofibrate displayed reductions in Hsd17b13 gene expression (q < 0.1). Associations of variants in SMAD3, IPO11, and HSD17B13, with gene expression changes in mice indicate that transforming growth factor‐beta (TGF‐β) and NRF2 signaling pathways may influence fenofibrate effects on dyslipidemia in patients with T2D. [ABSTRACT FROM AUTHOR]

Type 2 diabetes mellitus (T2DM), a metabolic disease becoming ever more common, is the result of disturbed glyco- and lipid metabolism. On the basis of their inhibitory effects against several key enzymes linked to T2DM, synthetic antidiabetic agents have been developed and used for diabetic therapy, some with adverse side effects. Fortunately, many plant non-starch polysaccharides (NSPs) have been shown to possess inhibitory effects on the same T2DM-related enzymes. Through a simple literature search we found that α-amylase, α-glucosidase, lipase, and dipeptidyl-peptidase IV are the enzymes most often reported in the context of T2DM. In this short review we discuss published evidence for inhibition of these enzymes and the implications for treating T2DM. [ABSTRACT FROM AUTHOR]

Introduction: Type 2 diabetes (T2D) is multifactorial involving lifestyle, environmental and genetic risk factors. This study aims to investigate the impact of genetic interactions with alcohol and diet quality on glycated haemoglobin A1c (HbA1c) independent of obesity, in a British population. Methods: Cross‐sectional study of 14 089 white British participants from Airwave Health Monitoring Study and a subsample of 3733 participants with dietary data. A T2D genetic risk score (GRS) was constructed, and its interactions with diet on HbA1c were assessed. Results: GRS was associated with a higher HbA1c% (β = 0.03, P < 0.0001) and a higher risk of prediabetes (OR = 1.09, P < 0.0001) and T2D (OR = 1.14, P = 0.006). The genetic effect on HbA1c% was significantly higher in obese participants (β = 1.88, Pinteraction = 0.03). A high intake of wholegrain attenuated the effect on HbA1c% in high‐risk individuals Pinteraction = 0.04. Conclusion: The genetic effect on HbA1c was almost doubled in obese individuals, compared with those with a healthy weight, and independent of weight, there was a modest offset on HbA1c in high‐genetic‐risk individuals consuming a diet high in wholegrain. This supports the importance of a healthy diet high in wholegrains and along with maintaining a healthy weight in controlling HbA1c among high‐genetic‐risk groups. [ABSTRACT FROM AUTHOR]