Zinc Supplementation and Strength Exercise in Rats with Type 2 Diabetes: Akt and PTP1B Phosphorylation in Nonalcoholic Fatty Liver

Vivero, Ariel; Ruz, Manuel; Miranda, Karen; Sacristán, Camila; Espinosa, Alejandra; Codoceo, Juana; Inostroza, Jorge; Vasquez, Karla; Pérez, A.; García-Díaz, Diego F.; Arredondo, Miguel

doi:10.1007/s12011-020-02324-3

Cited by 12 publications

(7 citation statements)

References 54 publications

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“…In this study, we assessed the effect of iAs on the primary insulin signaling pathway responsible for most of the metabolic actions of insulin, the phosphatidylinositol 3-kinase (PI3K)-AKT/protein kinase B (PKB) pathway [51] . The decrease or knockout of PTP1B, an enzyme that removes phosphate from tyrosine residues of cellular proteins, impairs insulin sensitivity through the downregulation of PEPCK, the enzyme catalyzing the formation of phosphoenolpyruvate, to alter the process of liver glycogen synthesis and gluconeogenesis [52] . We found that high iAs exposure signi cantly increased the level of ptp1b mRNA in both db/db and WT mice.…”

Section: Discussionmentioning

confidence: 99%

Effects of inorganic arsenic on type 2 diabetes mellitus in vivo: The roles and mechanisms of miRNAs

Sira

Zhang

Lin

et al. 2023

Preprint

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Accumulating studies have shown that chronic exposure to iAs correlates with an increased incidence of diabetes. In recent years, miRNA dysfunction has emerged both as a response to iAs exposure and independently as candidate drivers of metabolic phenotypes such as T2DM. However, few miRNAs have been profiled during the progression of diabetes after iAs exposure in vivo. In the present study, high iAs (10 mg/L NaAsO2) exposure mice models of C57BKS/Leprdb (db/db) and C57BLKS/J (WT) were established through the drinking water, the exposure duration was 14 weeks. The results showed that high iAs exposure induced no significant changes in FBG levels in either db/db or WT mice. FBI levels, C-peptide content and HOMA-IR levels were significantly increased, and glycogen levels in the livers were significantly lower in arsenic-exposed db/db mice. HOMA-β% was decreased significantly in WT mice exposed to high iAs. In addition, more different metabolites were found in the arsenic-exposed group than the control group in db/db mice, mainly involved in the lipid metabolism pathway. Highly expressed glucose, insulin, and lipid metabolism-related miRNAs were selected, including miR-29a-3p, miR-143-3p, miR-181a-3p, miR-122-3p, miR-22-3p and miR-16-3p. And a series of target genes were chosen for analysis, such as ptp1b, irs1, irs2, sirt1, g6pase, and pepck. The results showed that, the axles of miR-181a-3p-irs2, miR-181a-3p-sirt1, miR-22-3p-sirt1, and miR-122-3p-ptp1b in db/db mice, and miR-22-3p-sirt1, miR-16-3p-glut4 in WT mice could be considered as promising targets to explore the mechanisms and therapeutic aspects of T2DM after exposure to high iAs.

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Section: Discussionmentioning

confidence: 99%

Effects of inorganic arsenic on type 2 diabetes mellitus in vivo: The roles and mechanisms of miRNAs

Sira

Zhang

Lin

et al. 2023

Preprint

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“…In the setting of type 2 diabetes, the antioxidative effects of zinc supplementation were characterized by decreased hepatic MDA [ 45 ]. Another study showed that zinc supplementation in addition to strength exercise reduced the lipid accumulation under type 2 diabetic condition [ 46 ]. There has been no systematic study done to identify the role of zinc supplementation in the type 2 diabetes-induced hepatic damage that was investigated in the present study.…”

Section: Discussionmentioning

confidence: 99%

“…First, we investigated whether the above beneficial effect of zinc was attributed to the regulation of the glycemia and lipid metabolism. Previous studies demonstrated that zinc treatment did not improve, and even slightly enhanced the metabolic disorders [ 45 , 46 ]. Similar results were confirmed in this study, indicating that zinc supplementation-induced liver protection against type 2 diabetes was not attributed to the maintenance of glucose and lipid metabolism.…”

Section: Discussionmentioning

confidence: 99%

Zinc Supplementation Prevented Type 2 Diabetes-Induced Liver Injury Mediated by the Nrf2-MT Antioxidative Pathway

Liu

Jin

et al. 2021

Journal of Diabetes Research

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Zinc is an essential trace element that is often reduced under the type 1 diabetic condition. Previous studies demonstrated that zinc deficiency enhanced type 1 diabetes-induced liver injury and that zinc supplementation significantly helped to prevent this. Due to the differences in pathogenesis between type 1 and type 2 diabetes, it is unknown whether zinc supplementation can induce a beneficial effect on type 2 diabetes-induced liver injury. This possible protective mechanism was investigated in the present study. A high-fat diet, along with a one-time dose of streptozotocin, was applied to metallothionein (MT) knockout mice, nuclear factor-erythroid 2-related factor (Nrf) 2 knockout mice, and age-matched wild-type (WT) control mice, in order to induce type 2 diabetes. This was followed by zinc treatment at 5 mg/kg body weight given every other day for 3 months. Global metabolic disorders of both glucose and lipids were unaffected by zinc supplementation. This induced preventive effects on conditions caused by type 2 diabetes like oxidative stress, apoptosis, the subsequent hepatic inflammatory response, fibrosis, hypertrophy, and hepatic dysfunction. Additionally, we also observed that type 2 diabetes reduced hepatic MT expression, while zinc supplementation induced hepatic MT expression. This is a crucial antioxidant. A mechanistic study showed that MT deficiency blocked zinc supplementation-induced hepatic protection under the condition of type 2 diabetes. This suggested that endogenous MT is involved in the hepatic protection of zinc supplementation in type 2 diabetic mice. Furthermore, zinc supplementation-induced hepatic MT increase was unobserved once Nrf2 was deficient, indicating that Nrf2 mediated the upregulation of hepatic MT in response to zinc supplementation. Results of this study indicated that zinc supplementation prevented type 2 diabetes-induced liver injury through the activation of the Nrf2-MT-mediated antioxidative pathway.

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“…The effects of exercise training are associated with increased expression or activity of proteins involved in insulin signaling, subsequently modulating glycogen synthase activity, glucose transporter expression in the muscle, and improving IR, inflammation, and oxidative stress in T2DM patients (25). In a study, the benefits of strength exercise have been shown in reducing hepatic triglyceride content among T2DM rats (26). Traditionally, moderate-intensity continuous training has been considered an effective method of training for improving health outcomes in T2DM patients; however, high-intensity interval training (HIIT) is a well-accepted alternative strategy that may serve as a way for some individuals to save time (27).…”

Section: Introductionmentioning

confidence: 99%

The effects of camelina sativa oil and high-intensity interval training on liver function and metabolic outcomes in male type 2 diabetic rats

Kavyani

Dehghan²,

Khani³

et al. 2023

Front. Nutr.

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ObjectivesThe purpose of this study was to evaluate the independent and combined effects of camelina sativa oil and high-intensity interval training (HIIT) on liver function, and metabolic outcomes in streptozotocin-induced diabetic rats.MethodsForty male Wistar rats were randomly assigned to five equal groups (8 per group): Normal control (NC), diabetic control (DC), diabetic + camelina sativa oil (300 mg/kg by oral gavage per day; D + CSO), diabetic + HIIT (running on a treadmill 5 days/week for 8 weeks; D + HIIT), diabetic + camelina sativa oil + HIIT (D + CSO + HIIT).ResultsIn all three intervention groups (D + CSO, D + HIIT, and D + CSO + HIIT) compared to the DC, hepatic TNF-α, MDA, and histopathology markers, decreased and hepatic PGC-1α, and PPAR-γ increased (p < 0.05). However, the effect of D + CSO was greater than D + HIIT alone. Hepatic TG decreased significantly in D + HIIT and D + CSO + HIIT compared to other groups (p < 0.001). Fasting plasma glucose in all three intervention groups (D + CSO, D + HIIT, and D + CSO + HIIT) and HOMA-IR in D + CSO and D + CSO + HIIT were decreased compared to DC (p < 0.001). Only hepatic TAC and fasting plasma insulin remained unaffected in the three diabetic groups (p < 0.001). Overall, D + CSO + HIIT had the largest effect on all outcomes.ConclusionsAt the doses and treatment duration used in the current study, combination of CSO and HIIT was beneficial for reducing liver function and metabolic outcomes other than CSO and HIIT alone.

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Zinc Supplementation and Strength Exercise in Rats with Type 2 Diabetes: Akt and PTP1B Phosphorylation in Nonalcoholic Fatty Liver

Cited by 12 publications

References 54 publications

Effects of inorganic arsenic on type 2 diabetes mellitus in vivo: The roles and mechanisms of miRNAs

Effects of inorganic arsenic on type 2 diabetes mellitus in vivo: The roles and mechanisms of miRNAs

Zinc Supplementation Prevented Type 2 Diabetes-Induced Liver Injury Mediated by the Nrf2-MT Antioxidative Pathway

The effects of camelina sativa oil and high-intensity interval training on liver function and metabolic outcomes in male type 2 diabetic rats

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