scholarly journals Inverse correlation between serum high‐molecular‐weight adiponectin and proinsulin level in a Japanese population: The Dynamics of Lifestyle and Neighborhood Community on Health Study

2020 ◽  
Vol 12 (1) ◽  
pp. 63-66
Author(s):  
Akinobu Nakamura ◽  
Hideaki Miyoshi ◽  
Shigekazu Ukawa ◽  
Koshi Nakamura ◽  
Takafumi Nakagawa ◽  
...  
Keyword(s):  
Molecular Weight ◽  
High Molecular Weight ◽  
Japanese Population ◽  
Inverse Correlation ◽  
Health Study ◽  
High Molecular Weight Adiponectin ◽  
Proinsulin Level

Abstract 056: Associations of Total and High-Molecular-Weight Adiponectin with All-Cause and Cardiovascular Mortality in Older Persons: The Cardiovascular Health Study (CHS)

Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Jorge R Kizer ◽  
David Benkeser ◽  
Alice M Arnold ◽  
Kenneth J Mukamal ◽  
Joachim H Ix ◽  
...  
Keyword(s):  
Older Adults ◽  
Molecular Weight ◽  
High Molecular Weight ◽  
Cardiovascular Health ◽  
Additive Model ◽  
Health Study ◽  
Cardiovascular Health Study ◽  
High Molecular Weight Adiponectin ◽  
Risk Of Death ◽  
Cvd Mortality

Background: Adiponectin (APN) is inversely related to incident cardiovascular disease (CVD) in healthy middle-aged cohorts, but the opposite has been observed among older populations or those with prevalent CVD, where higher APN imparts greater risk of CVD and death. Emerging data suggest, however, that the association of total APN with mortality in elders may be U-shaped. Methods: We tested the hypotheses that both total and high-molecular-weight (HMW) APN (r=0.94) manifest different relations with mortality in subgroups of older adults defined by the presence or absence of prior CVD or heart failure (HF)/atrial fibrillation (AF). Specifically, we hypothesized that total and HMW APN would show similar U-shaped associations with all-cause and CVD death in subjects without prevalent CVD or HF/AF (Group [Gp] 1; n= 3272), but would exhibit positive monotonic associations with these outcomes in subgroups with prevalent CVD but no HF/AF (Gp 2; n=1030), and with prevalent HF/AF (Gp 3; n=383). We addressed these questions in CHS, a population-based US cohort aged 65 and older, of whom 4715 had available samples since 1992–93. Associations were examined with general additive model plots, and modeled with linear splines. Results: During 16 years of follow-up, 1947 all-cause and 634 CVD deaths occurred in Gp 1, 802 and 375 in Gp 2, and 337 and 180 in Gp 3. There was evidence of effect modification by subgroup status for both outcomes (p≤0.034), with total and HMW APN showing significant departures from linearity in their relations with all-cause and CVD mortality in Gp 1 (p≤0.043), but not Gps 2 or 3. The association between total APN and all-cause mortality was U-shaped, such that after adjustment for potential confounders, increasing levels up to 12.4 mg/L (median) were associated with a lower risk of death (HR 0.81 per SD [0.65–0.95]), but above this cutpoint, higher levels imparted a higher risk (HR 1.19 per SD [1.12–1.27]). Further adjustment for putative mediators (glucose, lipids, inflammation) abolished the association in the lower range, but left that in the upper range unaffected. The relationship was largely similar for HMW adiponectin. No significant association between total or HMW APN with mortality was apparent in Gp 2. In Gp 3, both total and HMW APN showed positive adjusted associations with mortality across their distributions, which were magnified after inclusion of putative mediators (HRs 1.31 [1.15–1.50] and 1.36 [1.20–1.55], respectively). Results were comparable for CVD mortality in all Gps. Conclusions: These findings show that total and HMW APN bear similar associations with all-cause and CVD mortality in older adults, and that these differ according to prevalent CVD or HF/AF status. These observations provide a potential explanation for the APN paradox, underscoring the need to better characterize the underpinnings of the hormone’s beneficial and harmful associations.

scholarly journals Acute and Short-term Chronic Testosterone Fluctuation Effects on Glucose Homeostasis, Insulin Sensitivity, and Adiponectin: A Randomized, Double-Blind, Placebo-Controlled, Crossover Study

2014 ◽  
Vol 99 (6) ◽  
pp. E1088-E1096 ◽  
Author(s):  
Christian Høst ◽  
Lars C. Gormsen ◽  
David M. Hougaard ◽  
Jens S. Christiansen ◽  
Steen B. Pedersen ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Glucose Metabolism ◽  
Crossover Study ◽  
High Molecular Weight ◽  
Glucose Disposal ◽  
Short Term ◽  
High Molecular Weight Adiponectin ◽  
Double Blind ◽  
Double Blind Placebo ◽  
Total Glucose

Context: Low levels of adiponectin and T in men have been shown to predict development of the metabolic syndrome, but the effects of T on glucose metabolism are incompletely understood and may be influenced either directly or indirectly through changes in body composition or in levels of adiponectin. Objective: The aim of the study was to test whether T exerts its effects on glucose metabolism directly or indirectly. Design, Setting, and Participants: In a randomized, double-blind, placebo-controlled, crossover study, 12 healthy young males were studied on four separate occasions. They received GnRH agonist treatment 1 month before 3 of 4 trial days to induce castrate levels of T. On trial days, T gel containing either high or low physiological T dose or placebo was applied to the body. On a fourth trial day, participants constituted their own eugonadal controls. Intervention: Each study comprised a 5-hour basal period and a 3-hour hyperinsulinemic euglycemic clamp. Main Outcome Measures: We measured the effect of acute T on peripheral glucose disposal, total adiponectin and subforms, and other indices of glucose metabolism. Results: Short-term hypogonadism was associated with increased high molecular weight adiponectin levels (P < .03) and increased oxidative glucose disposal (P = .03) but not total glucose disposal (P = .07). Acute T treatment was an independent suppressor of high molecular weight adiponectin levels (P = .04) but did not affect total glucose disposal (P = .17). Conclusions: These data show that T can act through putative fast nongenomic pathways to affect adiponectin levels in humans. The early hypogonadal state is characterized by a marked shift in fuel oxidation from lipids toward glucose, which may rely partly on buffering capabilities of adiponectin.

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