Title | Plasma lactate and diabetes risk in 8045 participants of the atherosclerosis risk in communities study. |
Publication Type | Journal Article |
Year of Publication | 2013 |
Authors | Juraschek SP, Selvin E, Miller ER, Brancati FL |
Secondary Authors | Young HJ |
Journal | Ann Epidemiol |
Volume | 23 |
Issue | 12 |
Pagination | 791-796.e4 |
Date Published | 2013 Dec |
ISSN | 1873-2585 |
Keywords | Adult, Aged, Atherosclerosis, Biomarkers, Blood Glucose, Community-Based Participatory Research, Diabetes Mellitus, Type 2, Female, Follow-Up Studies, Humans, Incidence, Insulin, Insulin Resistance, Lactic Acid, Male, Middle Aged, Proportional Hazards Models, Prospective Studies, Residence Characteristics, Risk Factors, United States |
Abstract | PURPOSE: Determinants of oxidative capacity, such as fitness and level of adiposity, are strongly associated with type 2 diabetes. Whether decreased oxidative capacity itself is a cause or consequence of insulin resistance and diabetes is unknown. METHODS: We examined the association of plasma lactate, a marker of oxidative capacity, with incident diabetes in 8045 participants from the Atherosclerosis Risk in Communities (ARIC) Study with no history of subclinical or diagnosed diabetes at baseline (1996-1998). Incident diabetes was self-reported during annual telephone calls. RESULTS: During a median follow-up of 12 years, there were 1513 new cases of diabetes. In Cox proportional hazards models, baseline plasma lactate (per 10 mg/dL) was significantly associated with diabetes (hazard ratio, 1.20; 95% confidence interval, 1.01-1.43), even after adjustment for diabetes risk factors, fasting glucose, and insulin. The upper quartile of baseline lactate (≥ 8.1 mg/dL) was also significantly associated with diabetes risk (hazard ratio, 1.20; 95% confidence interval, 1.02-1.41) compared with the lowest quartile (≤ 5.1 mg/dL). Significant associations persisted among persons without insulin resistance (homeostatic model assessment insulin resistance index CONCLUSIONS: These findings suggest that low oxidative capacity may precede diabetes. Future studies should evaluate the physiological origins of elevated lactate to better understand its possible role in the pathogenesis of diabetes. |
DOI | 10.1016/j.annepidem.2013.09.005 |
Alternate Journal | Ann Epidemiol |
PubMed ID | 24176820 |
PubMed Central ID | PMC4034672 |
Grant List | HHSN268201100005C / / PHS HHS / United States R01DK085458 / DK / NIDDK NIH HHS / United States HHSN268201100009C / / PHS HHS / United States P30 DK079637 / DK / NIDDK NIH HHS / United States T32 HL007024 / HL / NHLBI NIH HHS / United States HHSN268201100010C / / PHS HHS / United States 5P60DK079637-04 / DK / NIDDK NIH HHS / United States HHSN268201100008C / / PHS HHS / United States HHSN268201100012C / / PHS HHS / United States R01 DK085458 / DK / NIDDK NIH HHS / United States P60 DK079637 / DK / NIDDK NIH HHS / United States T32HL007024 / HL / NHLBI NIH HHS / United States HHSN268201100007C / / PHS HHS / United States HHSN268201100009C / HL / NHLBI NIH HHS / United States HHSN268201100011C / / PHS HHS / United States HHSN268201100006C / / PHS HHS / United States |