Differential unfolded protein response in skeletal muscle from non-diabetic glucose tolerant or intolerant patients with obesity before and after bariatric surgery

Marciniak, Camille; Duhem, Christian; Boulinguiez, Alexis; Raverdy, Violeta; Baud, Grégory; Verkindt, Hélène; Caïazzo, Robert; Staels, Bart; Duez, Hélène; Pattou, François; Lancel, Steve

doi:10.1007/s00592-020-01490-z

Cited by 3 publications

(2 citation statements)

References 36 publications

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“…Glucose-regulated protein 78 (GRP78) is an ER chaperone that is involved in protein folding and initiation of the UPR by binding to misfolded proteins. GRP78 expression is known to be increased in the skeletal muscle of glucose-intolerant patients with obesity and was positively correlated with fasting glucose levels [ 9 ]. The expression of ER stress markers in adipocytes is higher in obese human subjects than that in lean controls, and is correlated with body mass index and fat mass [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

Methionine sulfoxide reductase B3 deficiency inhibits the development of diet-induced insulin resistance in mice

et al. 2021

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Oxidative and endoplasmic reticulum (ER) stress are involved in mediating high-fat diet (HFD)-induced insulin resistance. As the ER-localized methionine sulfoxide reductase B3 (MsrB3) protects cells against oxidative and ER stress, we hypothesized that MsrB3 might be associated with HFD-induced insulin resistance. To test this hypothesis, we examined the effect of MsrB3 deficiency on HFD-induced insulin resistance using MsrB3 knockout (KO) mice. Mice were fed a control diet or HFD for 12 weeks and insulin sensitivity was measured using a hyperinsulinemic-euglycemic clamp. HFD consumption increased the body weight of both wild-type and MsrB3 KO mice, and no significant difference was observed between the genotypes. The HFD increased oxidative stress and induced insulin resistance in the skeletal muscle of wild-type mice, but did not affect either in MsrB3 KO mice. The unfolded protein response (UPR) was increased in MsrB3 KO mice upon consumption of HFD, but not in wild-type mice. Mitochondrial oxidative phosphorylation proteins and the levels of superoxide dismutase 2 and glutathione peroxidase 1 were increased in MsrB3 KO mice upon HFD consumption. The respiratory control ratio was reduced in wild-type mice consuming HFD but not in MsrB3 KO mice. The levels of calcium/calmodulin-dependent protein kinase kinase β, phosphorylated AMP-activated protein kinase, and peroxisome proliferator-activated receptor gamma coactivator 1α were increased in MsrB3 KO mice following HFD consumption. These results suggest that MsrB3 deficiency inhibits HFD-induced insulin resistance, and the increased mitochondrial biogenesis and antioxidant induction might be the mechanisms underlying this phenomenon.

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Section: Introductionmentioning

confidence: 99%

Methionine sulfoxide reductase B3 deficiency inhibits the development of diet-induced insulin resistance in mice

et al. 2021

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“…The UPR is normally activated in order to restore cell homeostasis and cell survival [71]. The increased expression of UPR was found in adipocytes and skeletal muscle of obese persons and glucose intolerant individuals, whereas their expressions were modulated by weight reduction [72,73]. The intimate link between the increased UPR activity and the impaired insulin signaling transduction has been addressed.…”

Section: ) Oxidative Stressmentioning

confidence: 99%

Efficacy and safety of mulberry leaves on glycemic control in patients with obesity and patients with type 2 diabetes

Boonchoo¹

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This work was divided into three study phases: the two-phase randomized controlled clinical trials and proteomics study. First, the phase I clinical trial aimed to determine efficacy and safety of mulberry leaves on postprandial glucose following the 50-g sucrose ingestion in healthy nondiabetic adults and to explore the optimal administered dose of 1-deoxynojirimycin (DNJ), the major antihyperglycemic compound of mulberry leaves. The results showed the alleviation of postprandial hyperglycemia by mulberry leaves in a dose-dependent fashion. Adverse effects of mulberry leaves included bloating and flatulence, loose stool, and nausea. In addition, 12 mg of DNJ was considered the optimal dose defined by the clinically effective dose with the minimal side effects. Second, the phase II clinical trial was conducted to determine efficacy and safety of the long-term administration of mulberry leaves on glycemic control in patients with obesity and patients with type 2 diabetes. Daily administration of mulberry leaves containing 12 mg of DNJ thrice daily before meals resulted in the improvement in glycemic control as well as insulin sensitivity in the mulberry leaves-treated group; however, there was no difference between the treatment group and the control. Moreover, mulberry leaves were capable of reducing blood lipids when compared with the control group. Our study did not observe the changes in hepatic and renal function by mulberry leaves administration. Nonetheless, it caused bloating and flatulence, loose stool, and constipation. Last, effects of mulberry leaves on expressions of plasma proteins of persons who enrolled the phase II clinical study were further determined using proteomics analysis. In response to mulberry leaves treatment, the analysis found modulation in expressions of proteins involved in metabolic regulation, extracellular matrix constituents and organization, immunity, and inflammatory response.

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Unstressing the Reticulum: Nutritional Strategies for Modulating Endoplasmic Reticulum Stress in Obesity

Brito,

Coutinho‐Wolino,

Almeida

et al. 2024

Molecular Nutrition Food Res

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The progression of obesity involves several molecular mechanisms that are closely associated with the pathophysiological response of the disease. Endoplasmic reticulum (ER) stress is one such factor. Lipotoxicity disrupts endoplasmic reticulum homeostasis in the context of obesity. Furthermore, it induces ER stress by activating several signaling pathways via inflammatory responses and oxidative stress. ER performs crucial functions in protein synthesis and lipid metabolism; thus, triggers such as lipotoxicity can promote the accumulation of misfolded proteins in the organelle. The accumulation of these proteins can lead to metabolic disorders and chronic inflammation, resulting in cell death. Thus, alternatives, such as flavonoids, amino acids, and polyphenols that are associated with antioxidant and anti‐inflammatory responses have been proposed to attenuate this response by modulating ER stress via the administration of nutrients and bioactive compounds. Decreasing inflammation and oxidative stress can reduce the expression of several ER stress markers and improve clinical outcomes through the management of obesity, including the control of body weight, visceral fat, and lipid accumulation. This review explores the metabolic changes resulting from ER stress and discusses the role of nutritional interventions in modulating the ER stress pathway in obesity.

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Differential unfolded protein response in skeletal muscle from non-diabetic glucose tolerant or intolerant patients with obesity before and after bariatric surgery

Cited by 3 publications

References 36 publications

Methionine sulfoxide reductase B3 deficiency inhibits the development of diet-induced insulin resistance in mice

Methionine sulfoxide reductase B3 deficiency inhibits the development of diet-induced insulin resistance in mice

Efficacy and safety of mulberry leaves on glycemic control in patients with obesity and patients with type 2 diabetes

Unstressing the Reticulum: Nutritional Strategies for Modulating Endoplasmic Reticulum Stress in Obesity

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