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Associations of leptin and adiponectin with incident type 2 diabetes and interactions among African Americans: the Jackson heart study

Authors
  • Bidulescu, Aurelian1
  • Dinh, Paul C. Jr1
  • Sarwary, Shabir1
  • Forsyth, Emily1
  • Luetke, Maya C.1
  • King, David B.2
  • Liu, Jiankang3
  • Davis, Sharon K.4
  • Correa, Adolfo5
  • 1 Indiana University School of Public Health, 1025 E. 7th Street, Bloomington, IN, 47405, USA , Bloomington (United States)
  • 2 Henry M Jackson Foundation for the advancement of Military Medicine, Bethesda, MD, USA , Bethesda (United States)
  • 3 Brigham and Women’s Hospital, Boston, MA, USA , Boston (United States)
  • 4 National Human Genome Research Institute, Genomics of Metabolic, Cardiovascular and Inflammatory Disease Branch, Social Epidemiology Research Unit, Bethesda, MD, USA , Bethesda (United States)
  • 5 Jackson Heart Study at University of Mississippi Medical Center, Jackson, MS, USA , Jackson (United States)
Type
Published Article
Journal
BMC Endocrine Disorders
Publisher
Springer (Biomed Central Ltd.)
Publication Date
Mar 04, 2020
Volume
20
Issue
1
Identifiers
DOI: 10.1186/s12902-020-0511-z
Source
Springer Nature
Keywords
License
Green

Abstract

BackgroundGrowing evidence suggests that leptin is critical for glycemic control. Impaired leptin signaling may also contribute to low adiponectin expression in obese individuals. We assessed the association of leptin and adiponectin with incident type 2 diabetes (T2D), their interactions with sex and obesity status, and mediation by insulin resistance.MethodsWe included study participants from the Jackson Heart Study, a prospective cohort of adult African Americans in Jackson, Mississippi, that were free of T2D at the baseline Exam 1. Incident T2D was defined as new cases at Exam 2 or Exam 3. We created separate Cox regression models (hazard ratios per log-transformed ng/mL of leptin and adiponectin) with and without insulin resistance, HOMA-IR. Mediation by insulin resistance was analyzed. Several interactions were assessed, including by sex, HbA1c, and obesity.ResultsAmong our 3363 participants (mean age 53 years, 63% women), 584 developed incident T2D. Leptin was directly associated with incident T2D when modeled without HOMA-IR (HR = 1.29, 95% CI = 1.05–1.58). This direct association between leptin and T2D was significant among men (HR = 1.33, 95% CI = 1.05–1.69), but nonsignificant among women (HR = 1.24, 95% CI = 0.94–1.64); statistical interaction with sex was nonsignificant (p = 0.65). The associations in all participants and in men were nullified by HOMA-IR (HR = 0.99, 95% CI = 0.80–1.22; HR = 1.00, 95% CI = 0.78–1.28, respectively), indicating mediation through insulin resistance (proportion mediated: 1.04), and were not observed in abdominally obese participants. Adiponectin was inversely associated with T2D even after adjustment for HOMA-IR in women (HR = 0.68, 95% CI = 0.55–0.84), but not in men (HR = 0.80, 95% CI = 0.62–1.04). The inverse association was present only among abdominally obese participants, and persisted after adjustment for HOMA-IR.ConclusionsAmong African Americans in the Jackson Heart Study the association of leptin with incident type 2 diabetes was mediated by insulin resistance. This association was present only among abdominally non-obese participants. Differences by sex appeared: men showed a significant association mediated by insulin resistance. Among abdominally obese participants, adiponectin was inversely associated with incident T2D even after adjustment for HOMA-IR. Our results should inform future clinical trials that aim to reduce the burden of type 2 diabetes through the modification of serum levels of leptin and adiponectin.

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