scholarly journals Cardiovascular risk of adipokines: a review

2017 ◽  
Vol 46 (6) ◽  
pp. 2082-2095 ◽  
Author(s):  
Frédéric Dutheil ◽  
Brett Ashley Gordon ◽  
Geraldine Naughton ◽  
Edward Crendal ◽  
Daniel Courteix ◽  
...  

Over the last two decades, the understanding of adipose tissue has undergone radical change. The perception has evolved from an inert energy storage tissue to that of an active endocrine organ. Adipose tissue releases a cluster of active molecules named adipokines. The severity of obesity-related diseases does not necessarily correlate with the extent of body fat accumulation but is closely related to body fat distribution, particularly to visceral localization. There is a distinction between the metabolic function of central obesity (visceral abdominal) and peripheral obesity (subcutaneous) in the production of adipokines. Visceral fat accumulation, linked with levels of some adipokines, induces chronic inflammation and metabolic disorders, including glucose intolerance, hyperlipidaemia, and arterial hypertension. Together, these conditions contribute to a diagnosis of metabolic syndrome, directly associated with the onset of cardiovascular disease. If it is well known that adipokines contribute to the inflammatory profile and appetite regulation, this review is novel in synthesising the current state of knowledge of the role of visceral adipose tissue and its secretion of adipokines in cardiovascular risk.

Author(s):  
Julie A. Côté ◽  
Julie Lessard ◽  
Jacques Mailloux ◽  
Philippe Laberge ◽  
Caroline Rhéaume ◽  
...  

AbstractThe association between circulating androgen levels and fat distribution in women has been widely inconsistent among existing studies.We sought to investigate the relation between plasma adrenal and gonadal androgen levels and body fat distribution, as well as abdominal adipocyte characteristics.Paired omental and subcutaneous adipose tissue samples were surgically obtained from 60 women (age, 47±5 years; body mass index, 26±5 kg/mSignificant negative associations were found between plasma dihydrotestosterone (DHT) levels and total adiposity (body mass index, r=–0.35, p<0.05; fat mass, r=–0.31, p<0.05) as well as computed tomography assessments of abdominal adiposity (r=–0.30, p<0.05 and r=–0.44, p<0.005 for subcutaneous and visceral adipose tissue area, respectively). The association between DHT levels and visceral adipose tissue area was independent of total body fat mass. A significant negative association was also observed between plasma DHT and omental adipocyte diameter (r=–0.27, p<0.05). When expressed as the omental/subcutaneous ratio, heparin-releasable lipoprotein lipase activity was negatively and significantly related to plasma DHT, androstenedione, and dehydroepiandrosterone (DHEA) levels.Abdominally obese women with large, metabolically active omental adipocytes appear to be characterized by reduced endogenous levels of DHT. The assumption that high androgen levels are associated with an android body fat distribution pattern in women should be critically re-examined.


2015 ◽  
Vol 112 (14) ◽  
pp. 4363-4368 ◽  
Author(s):  
James E. N. Minchin ◽  
Ingrid Dahlman ◽  
Christopher J. Harvey ◽  
Niklas Mejhert ◽  
Manvendra K. Singh ◽  
...  

Genome-wide association studies have implicated PLEXIN D1 (PLXND1) in body fat distribution and type 2 diabetes. However, a role for PLXND1 in regional adiposity and insulin resistance is unknown. Here we use in vivo imaging and genetic analysis in zebrafish to show that Plxnd1 regulates body fat distribution and insulin sensitivity. Plxnd1 deficiency in zebrafish induced hyperplastic morphology in visceral adipose tissue (VAT) and reduced lipid storage. In contrast, subcutaneous adipose tissue (SAT) growth and morphology were unaffected, resulting in altered body fat distribution and a reduced VAT:SAT ratio in zebrafish. A VAT-specific role for Plxnd1 appeared conserved in humans, as PLXND1 mRNA was positively associated with hypertrophic morphology in VAT, but not SAT. In zebrafish plxnd1 mutants, the effect on VAT morphology and body fat distribution was dependent on induction of the extracellular matrix protein collagen type V alpha 1 (col5a1). Furthermore, after high-fat feeding, zebrafish plxnd1 mutant VAT was resistant to expansion, and excess lipid was disproportionately deposited in SAT, leading to an even greater exacerbation of altered body fat distribution. Plxnd1-deficient zebrafish were protected from high-fat-diet-induced insulin resistance, and human VAT PLXND1 mRNA was positively associated with type 2 diabetes, suggesting a conserved role for PLXND1 in insulin sensitivity. Together, our findings identify Plxnd1 as a novel regulator of VAT growth, body fat distribution, and insulin sensitivity in both zebrafish and humans.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Giada Ostinelli ◽  
Jerzy Adamski ◽  
André Tchernof

Abstract Background: Excess visceral adipose tissue accumulation on anatomical structures such as the greater omentum and mesentery are strong predictors of obesity-associated comorbidities (1). High glucocorticoid levels have been associated with body fat distribution and preferential visceral fat accumulation as well as features of the metabolic syndrome (MetS) (2). These effects are thought to be mediated by the glucocorticoid receptor, a nuclear receptor showing affinity for both glucocorticoids and mineralocorticoids. In this study, we examined plasma concentrations of glucocorticoids and mineralocorticoids in women with or without the MetS. In addition, we assessed the ability of these steroids to predict fat accumulation and features of the MetS. Methods: In a sample of 49 women (age 47 ± 4.99 years; BMI 26.4 ± 4.70 kg/m2), plasma concentrations of cortisol, 11-deoxycortisol, cortisone, aldosterone, corticosterone and 11-deoxycorticosterone were analyzed by electrospray ionization-liquid chromatography-tandem mass spectroscopy (ESI-LC-MS/MS). Metabolic parameters were assessed to establish the presence of the MetS using NCEP-III criteria. Subcutaneous and visceral adipocyte cell size was measured by histomorphometry. Results: We found HDL-triglycerides to be positively associated with levels of 11-deoxycorticosterone, 11-deoxycortisol, corticosterone, cortisone and cortisol (p&lt;0.05 for all). 11-deoxycorticosterone concentration was also negatively associated with waist circumference (-0.294, p&lt;0.05), LDL-cholesterol and LDL-triglyceride content (-0.264 and -0.362, p&lt;0.05) whereas cortisone level was positively associated with fasting glucose (0.3, p&lt;0.05). Our model including mineralocorticoids predicted systolic blood pressure (R2=0.303), while the one including glucocorticoids predicted HDL-cholesterol (R2=0.495). In addition, as expected, we found that women with the MetS were characterized by significantly higher percentage body fat and displayed subcutaneous and visceral adipocyte hypertrophy (p&lt;0.05). Interestingly, women with the MetS also showed a trend for lower plasma cortisol concentrations (p=0.07). Conclusion: Our data suggest that glucocorticoids and mineralocorticoids are associated with individual components of the MetS in women. (1) Tchernof et al.(2013), Physiol Rev, 93(1); (2) Constantinopoulos et al., (2015), Eur J Endocrinol, 172(1)


2014 ◽  
Vol 39 (4) ◽  
pp. 503-511 ◽  
Author(s):  
Nicole Villeneuve ◽  
Emilie Pelletier-Beaumont ◽  
Julie-Anne Nazare ◽  
Isabelle Lemieux ◽  
Natalie Alméras ◽  
...  

The objectives were to (i) measure the effects of a 1-year lifestyle modification program on body fat distribution/anthropometric variables; (ii) determine the interrelationships between changes in all these variables; and (iii) investigate whether there is a selective reduction in deep (DSAT) vs. superficial subcutaneous adipose tissue (SSAT) at the abdominal level following a 1-year lifestyle modification program. Anthropometric variables, body composition and abdominal and midthigh fat distribution were assessed at baseline and after 1 year in 109 sedentary, dyslipidemic and abdominally obese men. Reductions in anthropometric variables, skinfold thicknesses (except the trunk/extremity ratio) and fat mass as well as an increase in fat-free mass were observed after 1 year (p < 0.0001). Decreases in abdominal adipose tissue volumes were also noted (–23%, –26%, –18%, –19%, –17%, p < 0.0001 for total adipose tissue, visceral adipose tissue, subcutaneous adipose tissue, DSAT and SSAT, respectively). Adipose tissue areas at midthigh also decreased (–18%, –18%, –17%, p < 0.0001 for total, deep, and subcutaneous adipose tissue, respectively). A reduction (–9%, p < 0.0001) in low-attenuation muscle area and an increase (+1%, p < 0.05) in normal-attenuation muscle area were also observed. There was a positive relationship between changes in visceral adipose tissue and changes in DSAT (r = 0.65, p < 0.0001) or SSAT (r = 0.63, p < 0.0001). Although absolute changes in DSAT were greater than changes in SSAT, relative changes in both depots were similar, independent of changes in visceral adipose tissue. The 1-year lifestyle modification program therefore improved the body fat distribution pattern and midthigh muscle quality in abdominally obese men.


2009 ◽  
Vol 160 (5) ◽  
pp. 759-767 ◽  
Author(s):  
Tore Christiansen ◽  
Søren K Paulsen ◽  
Jens M Bruun ◽  
Kristian Overgaard ◽  
Steffen Ringgaard ◽  
...  

ObjectiveWeight loss with preferential effect on the visceral adipose tissue (VAT) depot could have important clinical benefits. In this study, we investigated the independent and combined effect of regular exercise and diet induced weight loss on body fat distribution.DesignRandomized control design of i) exercise-only (EXO; 12 weeks of exercise without diet-restriction), ii) hypocaloric-diet (DIO; 8 weeks of very low energy diet (VLED 600 kcal/day) followed by 4-weeks weight maintenance diet) and iii) hypocaloric-diet and exercise (DEX; 8 weeks VLED 800 kcal/day+a 4-week weight maintenance diet combined with exercise throughout the 12 weeks).SubjectsSeventy-nine obese males and females were included.MeasurementsBody fat distribution was quantified by magnetic resonance imaging (MRI)-technology.ResultsIn the EXO group, the weight loss (3.5 kg) and the relative reduction in VAT (18%) was significantly lower compared with the weight losses in the DIO and DEX groups (12.3 kg;P<0.01) and to the reduction in VAT (30–37%;P<0.01). In all the three groups, the relative reduction of VAT was higher as compared with the reduction in fat mass (FM; combining all fat depots determined by MRI;P<0.01 for all comparisons). The changes in VAT were associated with changes in FM and related to the initial VAT/FM ratio (r2=0.72;P<0.01).ConclusionExercise has no additional effects in reduction of the VAT depot, compared with the major effects of hypocaloric diet alone. In addition, the effects of exerciseper seon VAT are relatively limited. The effects on the VAT depot are closely associated with changes in total FM.


Author(s):  
Giada Ostinelli ◽  
Jinchu Vijay ◽  
Marie-Claude Vohl ◽  
Elin Grundberg ◽  
Andre Tchernof

Sci ◽  
2021 ◽  
Vol 3 (1) ◽  
pp. 13
Author(s):  
Raine Toivonen ◽  
Sanja Vanhatalo ◽  
Maija Hollmén ◽  
Eveliina Munukka ◽  
Anniina Keskitalo ◽  
...  

Toll-like receptor 5 ligand, flagellin, and vascular adhesion protein 1 (VAP-1) are involved in non-alcoholic fatty liver disease. This study aimed to determine whether VAP-1 mediates flagellin-induced hepatic fat accumulation. The effects of flagellin on adipocyte VAP-1 expression were first studied in vitro. Then, flagellin (100 ng/mouse) or saline was intraperitoneally injected into C57BL/6J (WT) and C57BL/6-Aoc3-/- (VAP-1 KO) mice on a high-fat diet twice a week every 2 weeks for 10 weeks. After that, the effects on inflammation, insulin signaling, and metabolism were studied in liver and adipose tissues. Hepatic fat was quantified histologically and biochemically. Because flagellin challenge increased VAP-1 expression in human adipocytes, we used VAP-1 KO mice to determine whether VAP-1 regulates the inflammatory and metabolic effects of flagellin in vivo. In mice, VAP-1 mediated flagellin-induced inflammation, leukocyte infiltration, and lipolysis in visceral adipose tissue. Consequently, an increased release of glycerol led to hepatic steatosis in WT, but not in KO mice. Flagellin-induced hepatic fibrosis was not mediated by VAP-1. VAP-1 KO mice harbored more inflammation-related microbes than WT mice, while flagellin did not affect the gut microbiota. Our results suggest that by acting on visceral adipose tissue, flagellin increased leukocyte infiltration that induced lipolysis. Further, the released glycerol participated in hepatic fat accumulation. In conclusion, the results describe that gut microbial flagellin through VAP-1 induced hepatic steatosis.


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