Abstract
Food-related disorders are increasingly common in developed societies, and the psychological component of these disorders has been gaining increasing attention. Both overnourishment with high-fat diets and perinatal undernourishment in mice have been linked to a higher motivation toward food, resulting in an alteration in food intake. Clusterin (CLU), a multifaced protein, is overexpressed in the nucleus accumbens (NAc) of over-fed rats, as well as in those that suffered chronic undernutrition. Moreover, an increase of this protein was observed in the plasma of obese patients with food addiction, suggesting the implication of CLU in this eating disorder. To characterize CLU’s cellular mechanisms, in vitro experiments of undernutrition were performed using dopaminergic SH-SY5Y cells. To mimic in vivo dietary conditions, cells were treated with different fetal bovine serum (FBS) concentrations, resulting in control (C group) diet (10% FBS), undernourishment (U group) diet (0.5% FBS), and undernourishment diet followed by restoration of control diet (UC group) (0.5 + 10% FBS). Undernourishment compromised cell viability and proliferation, and concomitantly increased CLU secretion as well as the cytosolic pool of the protein, while decreasing the mitochondrial level. The restoration of normal conditions tended to recover cell physiology, and the normal levels and distribution of CLU. This research study is a step forward toward the characterization of clusterin as a potential marker for food addiction and nutritional status.
Highlights
Food-related disorders are increasingly common in developed societies, and the psychological component of these disorders has been gaining increasing attention
All the experiments presented here were repeated independently at least three times. Both cell viability and proliferation are decreased by undernourishment without mitochondrial alterations SH-SY5Y cells were treated with fetal bovine serum (FBS)-restricted medium to mimic an under-protein diet, mainly based on the major protein content in FBS, albumin
The idea is based on our previous in vivo results showing evidence that CLU may play a role in food addiction and can potentially be considered as a biomarker
Summary
Food-related disorders are increasingly common in developed societies, and the psychological component of these disorders has been gaining increasing attention. Drug and food addictions share neurobiological and (http://creativecommons.org/licenses/by/4.0/),allowing third parties to copy and redistribute the material in any medium or format and to remix,transform,and build upon the material for any purpose, even commercially, provided the original work is properly cited and states its license These findings highlight the idea that ‘food addiction’ may be responsible for some types of obesity and eating disorders. A hypoglycosylated form of CLU is produced under endoplasmic reticulum stress and translocated to the mitochondria using the chaperone BiP (GRP78), where induces apoptosis [32] This anti-apoptotic role of intracellular CLU has been linked to its interaction with apoptosis-related proteins, Bax and Bcl-xL [33,34,35,36]
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