The novel adipokine WISP1 associates with insulin resistance and impairs insulin action in human myotubes and mouse hepatocytes

Hörbelt, Tina; Tacke, Christopher; Markova, Mariya; Wiza, Daniella Herzfeld de; Velde, Frederique Van de; Bekaert, Marlies; Nieuwenhove, Yves Van; Hornemann, Silke; Rödiger, Maria; Seebeck, Nicole; Friedl, Elisabeth; Jonas, Wenke; Thoresen, G. Hege; Kuß, Oliver; Rosenthal, Anke; Lange, Volker; Pfeiffer, Andreas F. H.; Schürmann, Annette; Lapauw, Bruno; Rudovich, Natalia; Pivovarova, O; Ouwens, D.M.

doi:10.1007/s00125-018-4636-9

Cited by 34 publications

(51 citation statements)

References 36 publications

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“…Serum concentration of the adipokine is elevated in obesity, irrespective of glycemia or insulin resistance status . This observation was reinforced in a different study, where WISP1 levels were found elevated in obese men irrespective of glycemic status compared with nonobese men . Additionally, the group showed that insulin signaling was impaired when hepatocytes were incubated with WISP1 due to inhibition of insulin receptor phosphorylation, other downstream regulators, and suppression of glycogenesis as well as gluconeogenesis.…”

Section: Adipokines and Therapies That Modulate Their Activitymentioning

confidence: 89%

Remodeling adipose tissue inflammasome for type 2 diabetes mellitus treatment: Current perspective and translational strategies

Banerjee

Singh

2019

Bioengineering & Transla Med

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Obesity-associated type 2 diabetes mellitus (T2DM) is characterized by low-grade chronic systemic inflammation that arises primarily from the white adipose tissue. The interplay between various adipose tissue-derived chemokines drives insulin resistance in T2DM and has therefore become a subject of rigorous investigation. The adipocytokines strongly associated with glucose homeostasis include tumor necrosis factor-α, various interleukins, monocyte chemoattractant protein-1, adiponectin, and leptin, among others. Remodeling the adipose tissue inflammasome in obesity-associated T2DM is likely to treat the underlying cause of the disease and bring significant therapeutic benefit. Various strategies have been adopted or are being investigated to modulate the serum/tissue levels of pro-and anti-inflammatory adipocytokines to improve glucose homeostasis in T2DM. These include use of small molecule agonists/inhibitors, mimetics, antibodies, gene therapy, and other novel formulations. Here, we discuss adipocytokines that are strongly associated with insulin activity and therapies that are under investigation for modulation of their levels in the treatment of T2DM.

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Section: Adipokines and Therapies That Modulate Their Activitymentioning

confidence: 89%

Remodeling adipose tissue inflammasome for type 2 diabetes mellitus treatment: Current perspective and translational strategies

Banerjee

Singh

2019

Bioengineering & Transla Med

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“…In insulin-sensitive tissue, WISP-1 decreases the phosphorylation of insulin receptor and protein kinase B (akt). As a consequence, glycogen synthesis is reduced in myotubes, and gluconeogenic genes are upregulated in hepatocytes 17 . Accordingly, we observed significant correlations of serum WISP-1 level with fasting insulin, HOMA-IR, waist circumference, BMI, and body fat percentage in a cross-sectional analysis ( Supplementary Fig.…”

Section: Discussionmentioning

confidence: 99%

Exercise intervention lowers aberrant serum WISP-1 levels with insulin resistance in breast cancer survivors: a randomized controlled trial

Chang

Kim

Kong

2020

Sci Rep

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Insulin resistance is associated with increased risk for and recurrence of breast cancer. Recently, Wnt1-inducible signaling pathway protein-1 (WISP-1) was reported to impair glucose metabolism and insulin sensitivity. In various cancer tissues, Wnt signaling is upregulated and induces further oncogenic and metastatic activity. However, the effects of exercise on serum levels of WISP-1 and its upstream β-catenin have not been studied in cancer patients. We investigated the effects of exercise training on Wnt signaling and insulin sensitivity in breast cancer survivors (BCS). This single-center trial randomized 46 BCS into either 12-week exercise or control groups (1:1), and included an additional 12 age-matched healthy women. Kinanthropometric parameters, serum Wnt signaling markers, and gluco-lipid profiles were evaluated before and after the intervention. Serum β-catenin and WISP-1 concentrations were significantly higher in BCS than in healthy subjects. There was a positive correlation between β-catenin and WISP-1 levels. Exercise training in BCS significantly reduced body fat and waist circumference and enhanced aerobic and muscular fitness. Exercise decreased β-catenin and WISP-1 levels and improved gluco-lipid profiles. There was a notable correlation between changes in HOMA-IR indexes and serum WISP-1, but not with β-catenin during the exercise intervention. In conclusion, a 12-week community-based exercise intervention resulted in significant reductions in serum β-catenin and WISP-1 levels, accompanied by favorable improvements in body composition, physical fitness, and biochemical parameters in BCS. We also highlight that this is the first report concerning effects of exercise on circulating β-catenin and WISP-1 levels and correlations between WISP-1 and insulin sensitivity, which could be important for determining prognoses for BCS. Exercise is an important adjunct therapy in the management of cancer for optimal recovery and prevention of treatment-associated complications. Exercise also improves clinical outcomes, including cardiorespiratory and musculoskeletal fitness and recovery from physical and cognitive fatigue 1-3. Hence, regular exercise in cancer survivors contributes to shortening the time to return-to-work and enhances quality of daily life 4,5. Although the clinical utility of exercise-oncology has consistently emerged as a critical component of lifestyle modification to improve survival and reduce risk of recurrence 6 , there is less evidence relating exercise to tumorigenesis-related factors, and the biologic mechanisms underlying this association remain unclear. Wingless and integration site growth factor (Wnt) signaling plays vital roles in numerous cellular processes, including development, differentiation, proliferation, apoptosis, cell motility, and maintenance of the stem cell niche 7. For instance, Wnt signaling is crucial for breast development during pregnancy and lactation. Despite its physiologic importance, aberrant Wnt signaling is closely linked to tumorigenesis such as the ...

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“…Eine Übersicht über diese Zusammenhänge findet sich bei Fasshauer et al [3]. In einer aktuellen Studie haben Hörbelt et al ein weiteres Adipokin (WISP1) identifiziert, das eine Insulinresistenz von Muskelzellen bewirken kann [4].…”

Section: Merkeunclassified

Vitamin D, Koenzym Q und Insulinresistenz

Schmidt¹,

Bayer²,

Mahler³

et al. 2019

Ernährung & Medizin

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ZusammenfassungDie große chronische Volkskrankheit Diabetes mellitus Typ 2 wird oft auch als Pandemie des 21. Jahrhunderts bezeichnet. Denn die Prävalenz dieser durch einen Mangel an Insulin im Blut gekennzeichneten Stoffwechselerkrankung wird allein in Deutschland auf mehr als 10 % der Bevölkerung geschätzt mit einer weiter steigenden Tendenz und einer hohen Dunkelziffer.

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The novel adipokine WISP1 associates with insulin resistance and impairs insulin action in human myotubes and mouse hepatocytes

Abstract: Circulating WISP1 levels and WISP1 expression in VAT are increased in obesity independent of glycaemic status. Furthermore, WISP1 impaired insulin signalling in muscle and liver cells.

Cited by 34 publications

References 36 publications

Remodeling adipose tissue inflammasome for type 2 diabetes mellitus treatment: Current perspective and translational strategies

Remodeling adipose tissue inflammasome for type 2 diabetes mellitus treatment: Current perspective and translational strategies

Exercise intervention lowers aberrant serum WISP-1 levels with insulin resistance in breast cancer survivors: a randomized controlled trial

Vitamin D, Koenzym Q und Insulinresistenz

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