OBJECTIVELow HDL cholesterol (HDL-C) and small HDL particle size may directly promote hyperglycemia. We evaluated associations of HDL-C, apolipoprotein A-I (apoA-I), and HDL-C/apoA-I with insulin secretion, insulin resistance, HbA 1c , and long-term glycemic deterioration, reflected by initiation of pharmacologic glucose control. RESEARCH DESIGN AND METHODSThe 5-year Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study followed 9,795 type 2 diabetic subjects. We calculated baseline associations of fasting HDL-C, apoA-I, and HDL-C/apoA-I with HbA 1c and, in those not taking exogenous insulin (n = 8,271), with estimated b-cell function (homeostasis model assessment of b-cell function [HOMA-B]) and insulin resistance (HOMA-IR). Among the 2,608 subjects prescribed lifestyle only, Cox proportional hazards analysis evaluated associations of HDL-C, apoA-I, and HDL-C/apoA-I with subsequent initiation of oral hypoglycemic agents (OHAs) or insulin. RESULTSAdjusted for age and sex, baseline HDL-C, apoA-I, and HDL-C/apoA-I were inversely associated with HOMA-IR (r = 20.233, 20.134, and 20.230; all P < 0.001; n = 8,271) but not related to HbA 1c (all P > 0.05; n = 9,795). ApoA-I was also inversely associated with HOMA-B (r = 20.063; P = 0.002; n = 8,271) adjusted for age, sex, and HOMA-IR. Prospectively, lower baseline HDL-C and HDL-C/apoA-I levels predicted greater uptake (per 1-SD lower: hazard ratio [HR] 1.13 [CI 1.07-1.19], P < 0.001; and HR 1.16 [CI 1.10-1.23], P < 0.001, respectively) and earlier uptake (median 12.9 and 24.0 months, respectively, for quartile 1 vs. quartile 4; both P < 0.01) of OHAs and insulin, with no difference in HbA 1c thresholds for initiation (P = 0.87 and P = 0.81). Controlling for HOMA-IR and triglycerides lessened both associations, but HDL-C/apoA-I remained significant. CONCLUSIONSHDL-C, apoA-I, and HDL-C/apoA-I were associated with concurrent insulin resistance but not HbA 1c . However, lower HDL-C and HDL-C/apoA-I predicted greater and earlier need for pharmacologic glucose control.

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Aims We aimed to determine the incidence, prevalence and mortality of type 1 diabetes (T1D) in Uzbekistan in children <15 years old. Methods In a prospective study from 1998 to 2014 the primary ascertainment of incidence, prevalence and mortality, and cause of death was via data collected by endocrinology dispensaries in Uzbekistan's 14 administrative divisions. A second data collection for 2008‐2010 from a national audit in 2011 was used to determine age structure. Results Over 1998‐2014 T1D prevalence roughly doubled (7.8 to 15.3/100,000 population aged <15 years, P = .10), following a doubling of incidence (1.5 to 3.1/100 000 < 15 years), a 5.6% annualized increase, P = .001), with a fall in mortality per 1000 patient years (24.5 to 2.0, P = .001). There was a female preponderance, with a male:female ratio of 0.89 in 2008‐2010. In every year, T1D incidence was highest in the 10‐14.99 year age‐group, although the proportion of diagnoses under 5 years of age increased from 6.0% of total diagnoses in 1998‐2002, to 13.4% in 2008‐2010. Peak age of onset in 2008‐2010 was 13 years. Notable regional variation was evident, with incidence being highest in Tashkent‐City (P = .005). The most common cause of death was chronic renal failure—responsible for 31 deaths in children <15 years during the study period. Conclusions Our results provide the first long‐term epidemiological data for T1D in Uzbekistan and the region. Uzbekistan is country of low but rising T1D incidence and prevalence, and falling mortality. Attention to improving clinical care is warranted, to reduce long‐term complications.