Role of Omentin, Vaspin, Cardiotrophin-1, TWEAK and NOV/CCN3 in Obesity and Diabetes Development

Escoté, Xavier; Gómez‐Zorita, Saioa; López-Yoldi, Miguel; Milton-Laskíbar, Iñaki; Fernández‐Quintela, Alfredo; Martínéz, J. Alfredo; Moreno-Aliaga, María J.; Portillo, Marı́a P.

doi:10.3390/ijms18081770

Cited by 96 publications

(71 citation statements)

References 165 publications

(256 reference statements)

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“…While most of the recent studies on vaspin have focused on its physiological function, only few studies have reported the basis for regulation of the vaspin gene [13,14]. Although vaspin mRNA expression of diabetic OLETF rats was restricted to visceral white adipose tissue, mouse vaspin mRNA was highly expressed in the liver.…”

Section: Discussionmentioning

confidence: 99%

Insulin induces expression of the hepatic <i>vaspin</i> gene

et al. 2020

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Visceral adipose tissue-derived serine protease inhibitor (vaspin), initially identified in the visceral adipose tissue, is an adipokine that improves endoplasmic reticulum stress in obesity or insulin sensitivity and glucose tolerance. However, the transcriptional regulation of the hepatic vaspin gene remains elusive. We have previously shown that CCAAT-enhancerbinding protein α, a transcription factor of the basic leucine zipper class, positively regulates the vaspin gene. The present study aimed to investigate the nutritional or hormonal regulators of vaspin expression in the liver. For the fasting and refeeding study, mice in the fasting group were subjected to fasting for 24 h and then sacrificed. Mice in the refeeding group were subjected to fasting for 24 h and then refed with a 50% (w/w) sucrose/MF diet for further 24 h and then sacrificed. For the streptozotocin (STZ) study, STZ (50 mg/kg) was intraperitoneally injected into C57BL/6JJc1 mice for 5 d. Hepatic vaspin was repressed due to fasting for 24 h and was induced upon refeeding with a high-sucrose diet. In studies on liver-specific C/ EBPα-deficient mice, C/EBPα was not involved in the induction of hepatic vaspin upon refeeding. In addition, the depletion of insulin by streptozotocin treatment markedly decreased hepatic vaspin expression. Finally, fasting-repressed vaspin expression in the liver was significantly increased by direct injection of insulin into fasting mice. In conclusion, our results suggest that insulin is a positive regulator of hepatic vaspin expression.

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Section: Discussionmentioning

confidence: 99%

Insulin induces expression of the hepatic <i>vaspin</i> gene

et al. 2020

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“…The therapeutic implications of this adipokine and others, is of great interest in the field of diabetes mellitus and obesity [32].…”

Section: Discussionmentioning

confidence: 99%

Impact of 2 Different Hypocaloric Diets on Serum Omentin Levels in Obese Subjects

Luis¹,

Izaola²,

Primo³

et al. 2018

Ann Nutr Metab

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Background and Aims: Omentin-1 might play a role in insulin resistance and obesity. This study is aimed at evaluating the influence of weight loss treatment on omentin-1 concentrations and other parameters after 2 different hypocaloric diets in obese subjects. Methods: A total of 239 obese subjects were randomly allocated during 12 weeks (Diet I – high-fat diet vs. Diet II – low fat diet), and their anthropometric and biochemical status were evaluated. Results: After dietary intervention, BMI, weight, fat mass, waist circumference, systolic blood, triglycerides, LDL cholesterol, insulin levels and homeostasis model assessment for insulin resistance decreased in a statistical manner from their base values. After consuming diet II (low fat diet), the omentin-1 levels increased in males (20 ± 14 ng/mL) and females (35 ± 19 ng/mL). No changes were observed in omentin-1 levels after consuming hypocaloric diet type I (high fat). The multiple regression analyses after weight loss with diet I adjusted by age and sex showed a statistical association between BMI kg/m² (Beta –0.33: 95% CI –4.58 to –0.11) and post-treatment omentin-1 levels. The analysis after weight loss with diet II showed a statistical association with BMI kg/m² (Beta –0.31: 95% CI –3.93 to –0.08) and insulin UI/L (Beta –0.25: 95% CI –4.63 to –0.05) with post-treatment omentin-1 levels. Conclusions: Our design showed a significant increase in serum omentin-1 levels after weight loss secondary to a low fat hypocaloric diet, in contrast to no changes following consuming a high fat hypocaloric diet.

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“…CT-1 is a member of the interleukin-6 superfamily, which is expressed in different tissues including the heart, vessels, skeletal muscle, liver, lung, adipose tissue, and kidney [58,59]. In the myocardium, CT-1 is produced by both cardiomyocytes and fibroblasts, exerting its action through the glycoprotein 130 (gp130)/ leukemia inhibitory factor receptor (LIFR) heterodimer.…”

Section: Cardiotrophin-1 41 Cardiotrophin-1 Induces Fibrosis and Infmentioning

confidence: 99%

Aldosterone/Mineralocorticoid Receptor Downstream Targets as Novel Therapeutic Targets to Prevent Cardiovascular Remodeling

Ibarrola¹,

Jaisser²,

López‐Andrés³

2019

Aldosterone-Mineralocorticoid Receptor - Cell Biology to Translational Medicine

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The incidence of heart failure (HF) is increasing because of aging of the population. Despite optimal therapy, patients with HF experience disease progression associated with high mortality rates. HF is still the first cause of hospital admission in subjects aged >65 years. The obvious solution for HF epidemics is to prevent new-onset HF with therapies directed specifically to mechanistic targets that are involved in the transition to HF. The mineralocorticoid receptor (MR) and its natural ligand, the hormone aldosterone (Aldo), play important roles during cardiac and arterial remodeling, but the underlying effects are still not understood. MR antagonists are highly recommended for treatment of systolic symptomatic HF. However, adverse effects limit their use in clinical practice. Galectin-3 (Gal-3), neutrophil gelatinase-associated lipocalin (NGAL), and cardiotrophin-1 (CT-1) have been identified as highly focused targets controlling downstream key MR-mediated HF mechanisms. Therefore, interfering with mechanistic pathways involved in downstream MR activation may provide therapeutic alternatives to MR antagonists. The aim of this review is to focus on the role of the MR biotargets in cardiovascular remodeling.

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Role of Omentin, Vaspin, Cardiotrophin-1, TWEAK and NOV/CCN3 in Obesity and Diabetes Development

Cited by 96 publications

References 165 publications

Insulin induces expression of the hepatic <i>vaspin</i> gene

Insulin induces expression of the hepatic <i>vaspin</i> gene

Impact of 2 Different Hypocaloric Diets on Serum Omentin Levels in Obese Subjects

Aldosterone/Mineralocorticoid Receptor Downstream Targets as Novel Therapeutic Targets to Prevent Cardiovascular Remodeling

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