Adipokine Profile and Insulin Sensitivity in Formerly Obese Women Subjected to Bariatric Surgery or Diet-Induced Long-term Caloric Restriction

Mitterberger, Michael; Mattesich, Monika; Klaver, Elise; Lechner, Stefan; Engelhardt, Timm Oliver; Larcher, Lorenz; Pierer, Gerhard; Piza‐Katzer, Hildegunde; Zwerschke, Werner

doi:10.1093/gerona/glq107

Cited by 33 publications

(25 citation statements)

References 45 publications

(75 reference statements)

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“…In our model of chronic energy deprivation (exercise induced energy deficiency and hypothalamic amenorrhea), visfatin levels also remained unchanged, even with the normalization of leptin levels through administration of metreleptin for up to 3 months. These results are consistent with the absence of a significant change in circulating visfatin following a long-term, calorie-restricted diet in women (42), as well as the absence of a significant difference in serum visfatin levels between untreated patients with anorexia nervosa and bulimia nervosa and healthy control subjects (43). …”

Section: Discussionsupporting

confidence: 84%

Circulating vaspin and visfatin are not affected by acute or chronic energy deficiency or leptin administration in humans

Kang

Magkos

Sienkiewicz

et al. 2011

European Journal of Endocrinology

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Objective Animal and in vitro studies indicate that leptin alleviates starvation-induced reduction in circulating vaspin and stimulates the production of visfatin. We thus examined whether vaspin and visfatin are affected by short- and long-term energy deprivation and leptin administration in human subjects in vivo. Design and Methods We measured circulating levels of vaspin and visfatin 1) before and after 72-h of starvation (leading to severe hypoleptinemia) with or without leptin administration in replacement doses in 13 normal-weight subjects, 2) before and after 72-h of starvation with leptin administration in pharmacological doses in 13 lean and obese subjects, 3) during chronic energy deficiency in 8 women with hypothalamic amenorrhea on leptin replacement for 3 months, and 4) during chronic energy deficiency in 18 women with hypothalamic amenorrhea on leptin replacement or placebo for 3 months. Results Acute starvation decreased serum leptin (to 21% of baseline values, P=0.002) but had no significant effect on vaspin and visfatin concentrations (P>0.05). Nor did normalization of leptin levels affect the concentrations of these two adipokines (P>0.9). Leptin replacement in women with hypothalamic amenorrhea did not significantly alter vaspin and visfatin concentrations, whether relative to baseline (P>0.15) or relative to placebo administration (P>0.9). Pharmacological doses of leptin did not affect circulating vaspin and visfatin concentrations (P>0.9). Conclusions Circulating vaspin and visfatin are not affected by acute or chronic energy deficiency leading to hypoleptinemia and are not regulated by leptin in human subjects, indicating that these adipocyte-secreted hormonal regulators of metabolism are independently regulated in humans.

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Section: Discussionsupporting

confidence: 84%

Circulating vaspin and visfatin are not affected by acute or chronic energy deficiency or leptin administration in humans

Kang

Magkos

Sienkiewicz

et al. 2011

European Journal of Endocrinology

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“…Human sWAT samples were taken from eight formerly obese Caucasian women undergoing routine abdominoplasty after long-term weight loss interventions at the Institute for Plastic and Reconstructive Surgery (Medical University Innsbruck, Austria) [14, 46]. The patients gave their informed written consent and had been approved by the ethical committee of Innsbruck Medical University, Austria, according to the Declaration of Helsinki.…”

Section: Methodsmentioning

confidence: 99%

Silencing of the small GTPase DIRAS3 induces cellular senescence in human white adipose stromal/progenitor cells

Ejaz

Mattesich

Zwerschke

2017

Aging

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Inhibition of Akt-mTOR signaling protects from obesity and extends life span in animals. In the present study, we analyse the impact of the small GTPase, GTP-binding RAS-like 3 (DIRAS3), a recently identified weight-loss target gene, on cellular senescence in adipose stromal/progenitor cells (ASCs) derived from human subcutaneous white adipose tissue (sWAT). We demonstrate that DIRAS3 knock-down (KD) in ASCs induces activation of Akt-mTOR signaling and proliferation arrest. DIRAS3 KD ASCs lose the potential to form colonies and are negative for Ki-67. Moreover, silencing of DIRAS3 results in a premature senescence phenotype. This is characterized by senescence-associated β-galactosidase positive enlarged ASCs containing increased p16INK4A level and activated retinoblastoma protein. DIRAS3 KD ASCs form senescence-associated heterochromatic foci as shown by increased level of γ-H2A.X positive foci. Furthermore, these cells express a senescence-associated secretory phenotype characterized by increased interleukin-8 secretion. Human DIRAS3 KD ASCs develop also a senescence phenotype in sWAT of SCID mice. Finally, we show that DIRAS3 KD in ASCs stimulates both adipogenic differentiation and premature senescence. In conclusion, our data suggest that silencing of DIRAS3 in ASCs and subsequently hyper-activation of Akt-mTOR drives adipogenesis and premature senescence. Moreover, differentiating ASCs and/or mature adipocytes may acquire features of cellular senescence.

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“…Adiponectin levels increase with age; however, patients who have diabetes or obesity show lower plasma APN (1,24,31). Several studies indicate there may be a survival advantage conferred by the beneficial cardiometabolic protective effects of APN (2, 4).…”

Section: Anti-inflammatory Effects Of Etmentioning

confidence: 99%

Exercise training improves endothelial function via adiponectin-dependent and independent pathways in type 2 diabetic mice

Lee

Park

Dellsperger

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Lee S, Park Y, Dellsperger KC, Zhang C. Exercise training improves endothelial function via adiponectin-dependent and independent pathways in type 2 diabetic mice. Am J Physiol Heart Circ Physiol 301: H306 -H314, 2011. First published May 20, 2011 doi:10.1152/ajpheart.01306.2010.-Type 2 diabetes (T2D) is a leading risk factor for a variety of cardiovascular diseases including coronary heart disease and atherosclerosis. Exercise training (ET) has a beneficial effect on these disorders, but the basis for this effect is not fully understood. This study was designed to investigate whether the ET abates endothelial dysfunction in the aorta in T2D. Heterozygous controls (m Lepr db ) and type 2 diabetic mice (db/db; Lepr db ) were either exercise entrained by forced treadmill exercise or remained sedentary for 10 wk. Ex vivo functional assessment of aortic rings showed that ET restored acetylcholine-induced endothelial-dependent vasodilation of diabetic mice. Although the protein expression of endothelial nitric oxide synthase did not increase, ET reduced both IFN-␥ and superoxide production by inhibiting gp91 phox protein levels. In addition, ET increased the expression of adiponectin (APN) and the antioxidant enzyme, SOD-1. To investigate whether these beneficial effects of ET are APN dependent, we used adiponectin knockout (APNKO) mice. Indeed, impaired endothelial-dependent vasodilation occurred in APNKO mice, suggesting that APN plays a central role in prevention of endothelial dysfunction. APNKO mice also showed increased protein expression of IFN-␥, gp91 phox , and nitrotyrosine but protein expression of SOD-1 and -3 were comparable between wild-type and APNKO. These findings in the aorta imply that APN suppresses inflammation and oxidative stress in the aorta, but not SOD-1 and -3. Thus ET improves endothelial function in the aorta in T2D via both APN-dependent and independent pathways. This improvement is due to the effects of ET in inhibiting inflammation and oxidative stress (APN-dependent) as well as in improving antioxidant enzyme (APN-independent) performance in T2D. cardiovascular disease; inflammation; superoxide; vascular biology TYPE 2 DIABETES (T2D) is associated with impairment in endothelial function characterized by impaired endothelial-dependent vasodilation, increased inflammatory cell, and platelet adhesion in both rodents and humans (22,32,41,42,54). Accumulating evidence suggests that endothelial dysfunction is an early stage of atherosclerosis (11,41). Thus endothelial dysfunction with inflammatory cell and platelet adhesion may contribute to the development of atherosclerosis in T2D. Even though the mechanisms responsible for endothelial dysfunction are not fully elucidated, previous studies indicate that a decrease in nitric oxide (NO) bioavailability may play a central role in endothelial dysfunction in T2D (32,36,54).In addition, oxidative stress and chronic inflammation are important pathogenic factors in many diseases including T2D and cardiovascular diseases (CVD) such as stroke, cor...

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Adipokine Profile and Insulin Sensitivity in Formerly Obese Women Subjected to Bariatric Surgery or Diet-Induced Long-term Caloric Restriction

Cited by 33 publications

References 45 publications

Circulating vaspin and visfatin are not affected by acute or chronic energy deficiency or leptin administration in humans

Circulating vaspin and visfatin are not affected by acute or chronic energy deficiency or leptin administration in humans

Silencing of the small GTPase DIRAS3 induces cellular senescence in human white adipose stromal/progenitor cells

Exercise training improves endothelial function via adiponectin-dependent and independent pathways in type 2 diabetic mice

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