Non-HDL Cholesterol as a Predictor for Incident Type 2 Diabetes in Community-dwelling Adults: Longitudinal Findings Over 12 Years

BackgroundNon-high-density lipoprotein cholesterol (non-HDL cholesterol) is a simple measure to analyze the total amount of proatherogenic lipoproteins in the blood and to predict development of cardiovascular disease. However, it is unclear whether non-HDL cholesterol has a relationship with incident type 2 diabetes. This study aimed to evaluate the association between non-HDL cholesterol and incident type 2 diabetes with a large-sample, community-based Korean cohort over a 12-year period.MethodsAmong the 10,038 total participants, 7,608 (3,662 men and 3,946 women) without diabetes were selected from the Korean Genome and Epidemiology Study (KoGES). Their non-HDL cholesterol level was calculated as [total cholesterol – HDL cholesterol] mg/dL and divided into quartiles. Newly developed type 2 diabetes was defined as any of the following: a fasting plasma glucose level ≥ 126 mg/dL; a plasma glucose level ≥ 200 mg/dL at two hours after a 75-g oral glucose tolerance test; a glycosylated hemoglobin level ≥ 6.5%; or current treatment with oral anti-diabetic medications or insulin therapy. The hazard ratios (HRs) with 95% confidence intervals (CIs) for incident type 2 diabetes were calculated using multivariate Cox proportional hazards regression models after adjusting for potentially confounding variables.ResultsIn total, 1,442 individuals (18.9%: 1442 of 7608) developed type 2 diabetes during the 12-year follow up period, with an incident rate of 3.0–5.0. Compared to the reference first quartile, the HRs (95% CIs) of incident type 2 diabetes for the second, third, and fourth quartiles increased in a dose-response manner after adjusting for potentially confounding variables, including the HOMA-IR insulin resistance marker.ConclusionNon-HDL cholesterol level at baseline can be a useful predictor of new-onset type 2 diabetes.

Diabetes in Patients With Pancreatic Neuroendocrine Neoplasms

ObjectiveDiabetes mellitus (DM) is probably a risk factor for pancreatic neuroendocrine neoplasms (PNENs). However, the prevalence of DM in PNEN patients remains inconclusive. In the present study we observed the prevalence of DM and possible risk factors in PNEN patients.MethodsAfter excluding those with insulinoma, a total of 197 patients with PNENs were included. The demographic data, pathological characteristics, and data of blood biochemical tests were recorded. DM was considered if there was evidence of a fasting plasma glucose level of ≥7.0 mmol/L or a 2-h plasma glucose level of ≥11.1 mmol/L, or a history of DM at the time of PNEN diagnosis. Impaired fasting glucose was considered if fasting plasma glucose level was between 6.1 and 7.0 mmol/L.ResultsThe prevalence of DM, new-onset DM, and impaired fasting glucose were 17.26, 9.14, and 7.1%, respectively. The prevalence of DM was 26.0% in patients ≥60 years old (19/73) and 12.1% in patients <60 years old. Multivariable logistic regression analysis demonstrated that age, tumor size, and nerve invasion were independent risk factors for DM and impaired fasting glucose + DM (p < 0.05). Age, organs and nerve invasion were independent risk factors for impaired fasting glucose. Low high-density lipoprotein (HDL) was also a risk factor for incident of DM (OR = 0.15, 95%CI: 0.03–0.66). G2/G3 was an independent risk factor for DM in women.ConclusionOur data shows that the prevalence of DM is 17.26% in patients with PNENs and is 26.0% in patients ≥60 years of age after excluding insulinoma. Age, nerve invasion, tumor size, and HDL are risk factors for DM in PNEN patients.

Central dopamine D2 receptors regulate plasma glucose levels in mice through autonomic nerves

Recent evidence suggests that the central nervous system (CNS) regulates plasma glucose levels, but the underlying mechanism is unclear. The present study investigated the role of dopaminergic function in the CNS in regulation of plasma glucose levels in mice. I.c.v. injection of neither the dopamine D1 receptor agonist SKF 38393 nor the antagonist SCH 23390 influenced plasma glucose levels. In contrast, i.c.v. injection of both the dopamine D2 receptor agonist quinpirole and the antagonist l-sulpiride increased plasma glucose levels. Hyperglycemia induced by quinpirole and l-sulpiride was absent in dopamine D2 receptor knockout mice. I.c.v. injection of quinpirole and l-sulpiride each increased mRNA levels of hepatic glucose-6-phosphatase and phosphoenolpyruvate carboxykinase, which are the key enzymes for hepatic gluconeogenesis. Systemic injection of the β2 adrenoceptor antagonist ICI 118,551 inhibited hyperglycemia induced by l-sulpiride, but not by quinpirole. In contrast, hyperglycemia induced by quinpirole, but not by l-sulpiride, was inhibited by hepatic vagotomy. These results suggest that stimulation of central dopamine D2 receptors increases plasma glucose level by increasing hepatic glucose production through parasympathetic nerves, whereas inhibition of central dopamine D2 receptors increases plasma glucose level by increasing hepatic glucose production through sympathetic nerves.