Glycemic load is associated with diabetes and prediabetes among middle-aged and elderly adults in Guangzhou, China.

BACKGROUND AND OBJECTIVES: Previous studies have obtained conflicting findings regarding the possible associations between glycemic load (GL) indices and diabetes. In the present study, we examined cross-sectional associations between several GL indices, including the total dietary GL, the energy-adjusted GL, and the prevalence of abnormal glucose metabolism, including prediabetes and diabetes. METHODS AND STUDY DESIGN: This study was conducted in Guangzhou, China from July 2011 to December 2011. It included 2,022 participants (602 men and 1,420 women), between 45 and 75 years of age. The prevalence of abnormal glucose metabolism was compared across the quartiles of GL indices to discover any potential linear correlations. Stratified analysis was conducted according to the body mass index (BMI) and waist circumference (WC) measurements. RESULTS: Energy-adjusted GL was positively associated with the prevalence of diabetes and the multivariable-adjusted estimate of the OR comparing the highest versus the lowest quartile was 2.50 (95% CI, 1.49-4.19). For the stratified analysis by sex, BMI or WC, similar associations were observed. For the overweight and obese (BMI ≥24.0 kg/m2) or centrally obese (WC ≥85 cm for men or ≥80 cm for women) participants, compared to participants in the lowest quartile of energy-adjusted GL, those in the highest quartile showed an increased risk of abnormal glucose metabolism. The OR estimates were 2.25 (95% CI: 1.45-3.52) and 1.54 (95% CI: 1.06-2.25), respectively. CONCLUSIONS: High dietary energy-adjusted GL is associated with the prevalence of diabetes as well as abnormal glucose metabolism among middle-aged and elderly adults.

A greater glycemic load reduction was associated with a lower diabetes risk in pre-diabetic patients who consume a high glycemic load diet.

Few prospective studies evaluating the association between dietary glycemic load (GL) and diabetes have accounted for changes in GL. However, the diet of patients could be modified in response to an awareness of pre-diabetes. The aim of this study was to examine the longitudinal associations between changes in GL and the incidence of diabetes among pre-diabetic patients. We hypothesized that subjects with low and high baseline GL would show different correlations with diabetes. A total of 493 pre-diabetic patients (142 men and 351 women) between 40 and 79 years of age were included in this study. Dietary records and oral glucose tolerance tests were conducted every year. The participants were divided into low- and high-GL groups based on baseline GL. During a median 4 years of follow-up, 108 incident cases of diabetes were identified. Among participants with a high baseline GL, the incidence of diabetes increased with decreasing GL reduction, and the multivariate-adjusted HR (95% CI) was 2.34 (1.27-4.29) when comparing the lowest to the highest tertiles; however, among those with a low baseline GL, no significant association was observed. Regardless of baseline GL status, the incidence of diabetes was higher in individuals with a high follow-up GL than in those with a low follow-up GL, and the multivariate-adjusted HR (95% CI) was 1.64 (1.09-2.45). In conclusion, a greater GL reduction was associated with a lower diabetes risk in pre-diabetic patients with a high dietary GL. In patients with pre-diabetes and a low dietary GL, further reductions in GL did not show any additional effects.

Effect of intensive insulin treatment on plasma levels of lipoprotein-associated phospholipase A2 and secretory phospholipase A2 in patients with newly diagnosed type 2 diabetes.

BACKGROUND: China has the highest absolute disease burden of diabetes worldwide. For diabetic patients, diabetes-related vascular complications are major causes of morbidity and mortality. The roles of lipoprotein-associated phospholipase A2 (Lp-PLA2) and secretory phospholipase A2 (sPLA2) as inflammatory markers have been recently evaluated in the pathogenesis of both diabetes and atherosclerosis. We aimed to determine the mechanism through which patients with newly diagnosed type 2 diabetes gain long-term vascular benefit from intensive insulin therapy by evaluating the change in Lp-PLA2 and sPLA2 levels after early intensive insulin treatment and its relevance with insulin resistance and pancreatic ß-cell function. METHODS: In total, 90 patients with newly diagnosed type 2 diabetes mellitus were enrolled. All patients received continuous subcutaneous insulin infusion (CSII) for approximately 2 weeks. Intravenous glucose-tolerance test (IVGTT) and oral glucose-tolerance test (OGTT) were performed, and plasma concentrations of Lp-PLA2 and sPLA2 were measured before and after CSII. RESULTS: Levels of Lp-PLA2 and sPLA2 were significantly higher in diabetic patients with macroangiopathy than in those without (P < 0.05). After CSII, the sPLA2 level decreased significantly in all diabetic patients (P < 0.05), while the Lp-PLA2 level changed only in those with macroangiopathy (P < 0.05). The area under the curve of insulin in IVGTT and OGTT, the acute insulin response (AIR3-5), early phase of insulin secretion (ΔIns30/ΔG30), modified ß-cell function index, and homeostatic model assessment for ß-cell function (HOMA-ß) increased after treatment even when adjusted for the influence of insulin resistance (IR; P < 0.001). The HOMA-IR was lower after treatment, and the three other indicators adopted to estimate insulin sensitivity (ISIced, IAI, and QUICKI) were higher after treatment (P < 0.05). Correlation analysis showed that the decrease in the Lp-PLA2 and sPLA2 levels was positively correlated with a reduction in HOMA-IR after CSII (P < 0.05). Additionally, multiple linear regression analysis showed that Lp-PLA2 and sPLA2 independently correlated with HOMA-IR (P < 0.05). CONCLUSIONS: Lp-PLA2 and sPLA2 are closely related to insulin resistance and macroangiopathy in diabetic patients. Intensive insulin therapy might help improve IR and protect against diabetic macroangiopathy by influencing the Lp-PLA2 and sPLA2 levels. TRIAL REGISTRATION: ChiCTR-TRC-10001618 2010 September 16.