Abdominal fat deposits determined by magnetic resonance imaging in relation to leptin and vaspin levels as well as insulin resistance in the general adult population

Genske, F.; Kühn, JP; Pietzner, Maik; Homuth, Georg; Rathmann, W; Grabe, Hans J.; Völzke, Henry; Wallaschofski, Henri; Friedrich, Nele

doi:10.1038/ijo.2017.187

Cited by 19 publications

(24 citation statements)

References 49 publications

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“…In line with our results, these studies have mainly presented inverse associations of SAT and VAT with adiponectin (17,18), as well as positive associations with leptin (10,17,18) and chemerin concentrations (4). The contribution of LFC to circulating adipokine concentrations was addressed in only a few studies that reported conflicting results (10,18). Differences in Figure 4 (A) Beta estimates from linear regression analyses (n = 4,116) for the associations of circulating adipokine concentrations with different metabolic parameters and blood pressure as well as (B) odds ratios from logistic regression analyses (n = 4,116) for the associations between circulating adipokine concentrations and metabolic syndrome (MetS) as well as its components.…”

Section: Fat Deposits and Adipokinessupporting

confidence: 92%

“…However, previous studies, which dealt with circulating adipokine concentrations in relation to behavioral risk factors and metabolic phenotypes in humans, mostly included only a small number of participants (2,3), just observed selected patient cohorts (2,3), or concentrated only on one or two specific adipokines (2,6,8). Furthermore, only a few human studies have investigated associations of circulating adipokine concentrations with fat deposits (2,4,10).…”

Section: Original Articlementioning

confidence: 99%

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Associations of a Panel of Adipokines with Fat Deposits and Metabolic Phenotypes in a General Population

Fischer

Völzke

Kassubek

et al. 2020

Obesity

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Objective: This study provides a comprehensive overview of the associations of five adipokines (adiponectin, chemerin, galectin-3, leptin, and resistin) with fat deposits, behavioral risk factors, and metabolic phenotypes. Methods: Using multivariable linear and logistic regression models, cross-sectional data from 4,116 participants of the population-based Study of Health in Pomerania were analyzed. Results: Participants with obesity showed higher chemerin, galectin-3, and leptin but showed lower adiponectin concentrations. Independently of other fat compounds, liver fat content, visceral adipose tissue, and subcutaneous adipose tissue (SAT) were inversely associated with adiponectin. Independent positive associations of liver fat content and SAT with chemerin as well as of SAT with galectin-3 and leptin were observed. Physically inactive participants had higher chemerin and leptin concentrations. Smokers had higher chemerin and galectin-3 as well as lower leptin. Alcohol consumption was associated with adiponectin (positive) and resistin (inverse). All adipokines were associated with at least one lipid marker. Associations with glucose metabolism were seen for adiponectin, chemerin, galectin-3, and leptin. Conclusions: High adiponectin concentrations were related to favorable metabolic conditions, whereas high chemerin, galectin-3, and leptin were associated with an unfavorable metabolic profile. High leptin seems to be primarily indicative of obesity, whereas high adiponectin and chemerin are associated with a broader range of metabolic phenotypes.

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Section: Fat Deposits and Adipokinessupporting

confidence: 92%

Section: Original Articlementioning

confidence: 99%

Associations of a Panel of Adipokines with Fat Deposits and Metabolic Phenotypes in a General Population

Fischer

Völzke

Kassubek

et al. 2020

Obesity

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show abstract

“…In this same study, leptin was not independently related to abdominal fat distribution and the authors concluded that circulating leptin climbs continuously with increasing adiposity [38]. A more recent study showed a strong positive association between subcutaneous adipose tissue and leptin levels, but not visceral adipose tissue nor liver fat content and leptin, independent of the HOMA-IR status [39]. Our finding of increased risk of type 2 diabetes with increased levels of leptin observed among abdominally non-obese participants adds weight to the "leptin resistance' phenomenon in the context of a large population sample.…”

Section: Discussionmentioning

confidence: 78%

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

et al. 2020

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Background: Growing 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. Methods: We 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. Results: Among 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. (Continued on next page)Conclusions: Among 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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“…[38] A more recent study showed a strong positive association between subcutaneous adipose tissue and leptin levels, but not visceral adipose tissue nor liver fat content and leptin, independent of the HOMA-IR status. [39] Our finding of increased risk of type 2 diabetes with increased levels of leptin observed among abdominally non-obese participants adds weight to the "leptin resistance' phenomenon in the context of a large population sample.…”

Section: Discussionmentioning

confidence: 57%

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

Bidulescu

Dinh

Sarwary

et al. 2020

Preprint

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Background: Growing 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. Methods: We 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. Results: Among our 3,363 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. Conclusions: Among African Americans in the Jackson Heart Study the association of leptin with incident type 2 diabetes was explained by HOMA-IR. The association of leptin and incident T2D was mediated by insulin resistance and present only among abdominally non-obese. 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.

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Abdominal fat deposits determined by magnetic resonance imaging in relation to leptin and vaspin levels as well as insulin resistance in the general adult population

Cited by 19 publications

References 49 publications

Associations of a Panel of Adipokines with Fat Deposits and Metabolic Phenotypes in a General Population

Associations of a Panel of Adipokines with Fat Deposits and Metabolic Phenotypes in a General Population

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

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

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