Delaying of insulin signal transduction in skeletal muscle cells by selenium compounds

Pinto, Antonio; Speckmann, Bodo; Heisler, Martin; Sies, Helmut; Steinbrenner, Holger

doi:10.1016/j.jinorgbio.2011.03.010

Cited by 43 publications

(22 citation statements)

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“…An elevated specific activity of GPx, however, would cause enhanced reduction of H 2 O 2 and thus interfere with this crucial local action of H 2 O 2 , rendering cells less responsive to insulin. Similar effects were observed in cultured cells exposed to selenocompounds fostering the cellular production of antioxidant selenoenzymes: insulin-induced signaling was attenuated [42].…”

Section: Stress Intracellular Signaling and Agingsupporting

confidence: 58%

Stress and biological aging

Simm

Klotz

2015

Z Gerontol Geriat

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It is well accepted that aging is the basis of most degenerative diseases in the elderly. Biological aging is characterized by a gradual accumulation of cellular and molecular defects. An important cause of defects is intense stress, such as oxidative or glycotoxic stress. Genes affecting cellular and organismal longevity are frequently associated with the regulation of cellular anti-oxidative defense and/or with repair functions. Damage, combined with an age-dependent decline in defense and repair systems, results in disturbed homeostasis, leading to aging and diseases. Whereas intense stress induces premature aging, mild stress can induce adaptive processes, stimulating the expression of genetic repair/defense systems, which positively influences life span.

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Section: Stress Intracellular Signaling and Agingsupporting

confidence: 58%

Stress and biological aging

Simm

Klotz

2015

Z Gerontol Geriat

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“…(activation) of protein kinase B (Akt) in hepatocytes and in myocytes (62,70), and conversely, insulin downregulates hepatic biosynthesis of SeP (62,83), thus providing a potential feedback loop. On the one hand, Akt integrates actions of insulin on energy metabolism, and its impaired activation may result in insulin resistance, a key feature of T2DM (77).…”

Section: Attenuation Of Akt-mediated Signaling By Se: Tradeoff Betweementioning

confidence: 99%

Toward Understanding Success and Failures in the Use of Selenium for Cancer Prevention

Steinbrenner

Speckmann

Sies

2013

Antioxidants & Redox Signaling

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Significance: Adequate and supranutritional selenium (Se) intake, maintaining full expression of selenoproteins, has been assumed to be beneficial for human health with respect to prevention of cancer. Strikingly, the effectiveness of dietary Se supplementation depends on many factors: baseline Se status, age, gender, and genetic background of an individual; type of cancer; and time point of intervention in addition to metabolic conversion and dose of applied Se compounds. Recent Advances: Se intake levels for optimization of plasma selenoproteins in humans have been delineated. Regulation, function, and genetic variants of several selenoproteins have been characterized in the intestine, where Se-mediated prevention of colorectal cancer appears to be particularly promising. Critical Issues: Numerous cell culture and animal studies indicate anticarcinogenic capacity of various Se compounds but, at present, the outcome of human studies is inconsistent and, in large part, disappointing. Moreover, supranutritional Se intake may even trigger adverse health effects, possibly increasing the risk for Type 2 diabetes in Se-replete populations. Future Directions: To improve protocols for the use of Se in cancer prevention, knowledge on cellular and systemic actions of Se compounds needs to be broadened and linked to individual-related determinants such as the occurrence of variants in selenoprotein genes and the Se status. Based on better mechanistic insight, populations and individuals that may benefit most from dietary Se supplementation need to be defined and studied in suitably planned intervention trials.

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“…Abundant expression of selenoproteins such as cytosolic glutathione peroxidase (GPx1) and selenoprotein P (SeP) can dysregulate insulin secretion and impair insulin sensitivity [6,[12][13][14]. Sodium selenite delayed insulin-induced phosphorylation of Akt and FoxO1a/3 in myocytes [15], and conversely, Akt phosphorylation was increased in skeletal muscle of transgenic mice with deficient selenoprotein biosynthesis [16].…”

Section: Introductionmentioning

confidence: 99%