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CGM use may be beneficial in insulin-treated GDM because it improves HbA compared with usual antenatal care without increasing severe hypoglycaemia. (Clinical Trials Registry No.: NCT02204657).

Background and Aim The recommendation in regard to screening for non‐alcoholic fatty liver disease (NAFLD) among type 2 diabetes mellitus (T2DM) patients differs in major guidelines. The aim of this paper was to study the prevalence of NALFD and advanced fibrosis among T2DM patients. Methods This is a cross‐sectional study of consecutive adult T2DM patients attending the Diabetes Clinic of a university hospital. Significant hepatic steatosis and advanced fibrosis was diagnosed based on transient elastography if the controlled attenuation parameter was ≥ 263 dB/m, and the liver stiffness measurement was ≥ 9.6 kPa using the M probe or ≥ 9.3 kPa using the XL probe, respectively. Patients with liver stiffness measurement ≥ 8 kPa were referred to the Gastroenterology and Hepatology Clinic for further assessment, including liver biopsy. Results The data of 557 patients were analyzed (mean age 61.4 ± 10.8 years, male 40.6%). The prevalence of NAFLD and advanced fibrosis based on transient elastography was 72.4% and 21.0%, respectively. On multivariate analysis, independent factors associated with NAFLD were central obesity (OR 4.856, 95% confidence interval [CI] 2.749–8.577, P = 0.006), serum triglyceride (OR 1.585, 95% CI 1.056–2.381, P = 0.026), and alanine aminotransferase levels (OR 1.047, 95% CI 1.025–1.070, P < 0.001) while advanced fibrosis was associated with serum high‐density lipoprotein cholesterol (OR 0.355, 95% CI 0.126–0.997, P = 0.049), alanine aminotransferase (OR 1.023, 95% CI 1.009–1.037, P = 0.001), γ‐glutamyltransferase (OR 1.005, 95% CI 1.001–1.008, P = 0.017), and platelet levels (OR 0.995, 95% CI 0.992–0.999, P = 0.010). Seventy‐one patients underwent liver biopsy. The majority had non‐alcoholic steatohepatitis (83.1%) and ≥ F1 fibrosis (87.3%) while advanced fibrosis was seen in 36.6%. Conclusion The prevalence of NAFLD and advanced fibrosis based on transient elastography is high among T2DM patients.

NAFLD was seen in half of a cohort of diabetic patients and was independently associated with central obesity and elevated serum ALT level. Prevalence of NAFLD was different and paralleled the difference in prevalence of central obesity and in percentage calorie intake from fat among the different ethnic groups.

ObjectiveTo explore factors influencing poor glycaemic control in people with type 2 diabetes using insulin.Research designA qualitative method comprising in-depth individual interviews. A semistructured interview guide was used. The interviews were audiorecorded, transcribed verbatim and analysed using a thematic approach.ParticipantsSeventeen people with type 2 diabetes using insulin with glycated haemoglobin (HbA1c) ≥9% for >1 year.SettingThe Primary Care Clinic and Diabetes Clinic in the University of Malaya Medical Centre (UMMC), Malaysia.ResultsData analysis uncovered four themes: lifestyle challenges in adhering to medical recommendations; psychosocial and emotional hurdles; treatment-related factors; lack of knowledge about and self-efficacy in diabetes self-care.ConclusionsFactors that explain the poor glycaemic control in people with type 2 diabetes using insulin were identified. Healthcare providers could use these findings to address patients’ concerns during consultations and help to improve glycaemic control.

Type 2 diabetes mellitus patients with coronary artery disease have become a major public health concern. The occurrence of insulin resistance accompanied with endothelial dysfunction worsens the state of atherosclerosis in type 2 diabetes mellitus patients. The combination of insulin resistance and endothelial dysfunction leads to coronary artery disease and ischemic heart disease complications. A recognized biological marker, high-sensitivity C-reactive protein, has been used widely to assess the progression of atherosclerosis and inflammation. Along with coronary arterial damage and inflammatory processes, high-sensitivity C-reactive protein is considered as an essential atherosclerosis marker in patients with cardiovascular disease, but not as an insulin resistance marker in type 2 diabetes mellitus patients. A new biological marker that can act as a reliable indicator of both the exact state of insulin resistance and atherosclerosis is required to facilitate optimal health management of diabetic patients. Malfunctioning of insulin mechanism and endothelial dysfunction leads to innate immune activation and released several biological markers into circulation. This review examines potential biological markers, YKL-40, alpha-hydroxybutyrate, soluble CD36, leptin, resistin, interleukin-18, retinol binding protein-4, and chemerin, as they may play significant roles in insulin resistance and atherosclerosis in type 2 diabetes mellitus patients with coronary artery disease.

Chemerin is one of the markers that may involve in development of both cancer and insulin resistance. Chemokine like receptor- 1 (CMKLR-1) receptor that regulates chemerin levels exhibits a potential therapeutic target for insulin resistance, type 2 diabetes and cancer treatment.

Generally, obese and overweight individuals display higher free fatty acid levels, which stimulate insulin resistance. The combination of overweight or obesity with insulin resistance can trigger Type 2 diabetes mellitus (T2DM) and are primary contributing factors to the development of uncontrolled T2DM. Genetic polymorphisms also play an important role as they can impact a population's susceptibility to becoming overweight or obese and developing related chronic complications, such as uncontrolled T2DM. This review specifically examines the genetic polymorphisms associated with overweight and obesity in patients with uncontrolled T2DM. Particularly, gene polymorphisms in ADIPOQ (rs1501299 and rs17300539), LepR (rs1137101 and rs1045895), IRS2 (rs1805092), GRB14 (rs10195252 and rs3923113) and PPARG (rs1801282) have been associated with overweight and obesity in uncontrolled T2DM.