Sucrose nonfermenting AMPK‐related kinase (SNARK) regulates exercise‐stimulated and ischemia‐stimulated glucose transport in the heart

Sun, Xianglan; Lessard, Sarah J.; Ding, An; Koh, Ho‐Jin; Esumi, Hiroyasu; Hirshman, Michael F.; Goodyear, Laurie J.

doi:10.1002/jcb.27425

Cited by 4 publications

(4 citation statements)

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“…Finally, RNA seq analysis of the liver revealed that treatment with HMH2 induced a 1.29-fold increase (0.37 log2 fold change) in Nuak2 transcript expression versus the HFHS diet control. Nuak2, also termed SNARK, has been identified as a mediator of insulin-independent glucose transport, specifically regulating exercise-and ischemia-stimulated glucose transport in the heart and contraction-stimulated glucose transport in skeletal muscle [56,57]. However, our understanding of SNARK's impact on glucose metabolism is still quite limited.…”

Section: Discussionmentioning

confidence: 99%

Animal and Cellular Studies Demonstrate Some of the Beneficial Impacts of Herring Milt Hydrolysates on Obesity-Induced Glucose Intolerance and Inflammation

et al. 2020

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The search for bioactive compounds from enzymatic hydrolysates has increased in the last few decades. Fish by-products have been shown to be rich in these valuable molecules; for instance, herring milt is a complex matrix composed of lipids, nucleotides, minerals, and proteins. However, limited information is available on the potential health benefits of this by-product. In this context, three industrial products containing herring milt hydrolysate (HMH) were tested in both animal and cellular models to measure their effects on obesity-related metabolic disorders. Male C57Bl/6J mice were fed either a control chow diet or a high-fat high-sucrose (HFHS) diet for 8 weeks and received either the vehicle (water) or one of the three HMH products (HMH1, HMH2, and HMH3) at a dose of 208.8 mg/kg (representing 1 g/day for a human) by daily oral gavage. The impact of HMH treatments on insulin and glucose tolerance, lipid homeostasis, liver gene expression, and the gut microbiota profile was studied. In parallel, the effects of HMH on glucose uptake and inflammation were studied in L6 myocytes and J774 macrophages, respectively. In vivo, daily treatment with HMH2 and HMH3 improved early time point glycemia during the oral glucose tolerance test (OGTT) induced by the HFHS diet, without changes in weight gain and insulin secretion. Interestingly, we also observed that HMH2 consumption partially prevented a lower abundance of Lactobacillus species in the gut microbiota of HFHS diet-fed animals. In addition to this, modulations of gene expression in the liver, such as the upregulation of sucrose nonfermenting AMPK-related kinase (SNARK), were reported for the first time in mice treated with HMH products. While HMH2 and HMH3 inhibited inducible nitric oxide synthase (iNOS) induction in J774 macrophages, glucose uptake was not modified in L6 muscle cells. These results indicate that milt herring hydrolysates reduce some metabolic and inflammatory alterations in cellular and animal models, suggesting a possible novel marine ingredient to help fight against obesity-related immunometabolic disorders.

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Section: Discussionmentioning

confidence: 99%

Animal and Cellular Studies Demonstrate Some of the Beneficial Impacts of Herring Milt Hydrolysates on Obesity-Induced Glucose Intolerance and Inflammation

et al. 2020

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“…Additionally, glucose uptake induced by exercise was abolished in heterozygous SNARK knockout mice. In HL1 cardiomyocytes, knockdown of SNARK resulted in a decreased glucose uptake and ischemia-induced phosphorylation of TBC1D4 at Ser711, while insulin-stimulated TBC1D4 phosphorylation was unaffected [70]. Collectively, the data suggest that SNARK may act in a pathway downstream of LKB1 to influence exercise-induced glucose uptake in skeletal muscle and the heart, presumably via phosphorylation of the RabGAPs.…”

Section: Snark and Ark5 Present Promising Upstream Kinases Of Tbc1d1 ...mentioning

confidence: 78%

“…Overexpression of mtSNARK and heterozygous SNARK whole-body knockout also led to reduced TBC1D4 and TBC1D1 phosphorylation induced by contraction (as determined using PAS antibody). Furthermore, heterozygous SNARK depletion reduced glucose uptake induced by in vitro contraction in soleus muscle and induced by treadmill exercise in gastrocnemius muscle [67,70]. Insulin-stimulated glucose uptake, however, remained unaltered by the overexpression of mtSNARK or heterozygous SNARK knockout [67].…”

Section: Snark and Ark5 Present Promising Upstream Kinases Of Tbc1d1 ...mentioning

confidence: 95%

“…Muscle specific ARK5 KO mice -Increased insulin-stimulated glucose uptake in soleus ex vivo -Increased phosphorylation of TBC1D4 Thr649 in soleus after glucose administration in mice on HFD [69] SNARK TA Muscle mtSNARK mice -Reduced contraction-stimulated glucose uptake in TA in situ -Reduced TBC1D1 and TBC1D4 phosphorylation in TA in situ [67] Heterozygous SNARK KO mice -Reduced contraction-stimulated glucose uptake in soleus in vitro -Reduced TBC1D1 and TBC1D4 phosphorylation after contraction in soleus in vitro [67] Heterozygous SNARK KO mice -Reduced treadmill exercise-stimulated glucose uptake in gastrocnemius and heart [67,70] HL1 (mouse cardio-myocyte cell line) SNARK knockdown -Reduced ischemia-induced glucose uptake HL1 cells -Reduced ischemia-induced TBC1D4 Ser711 phosphorylation in HL1 cells [70] Sik1-3 silencing in human adipocytes Reduced basal-and insulin-stimulated glucose uptake [71] SIK inhibition in human adipocytes with -HG-9-91-01 -YKL-05-099 -Reduced basal-and insulin-stimulated glucose uptake (Inhibitor: YKL-05-099 and HG-9-91-01) -Reduced insulin-stimulated TBC1D4 Thr642 phosphorylation (Inhibitor: HG-9-91-01) […”

Section: ] Ark5mentioning

confidence: 99%

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AMPK and Beyond: The Signaling Network Controlling RabGAPs and Contraction-Mediated Glucose Uptake in Skeletal Muscle

Peifer-Weiß,

Al-Hasani,

Chadt

2024

IJMS

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Impaired skeletal muscle glucose uptake is a key feature in the development of insulin resistance and type 2 diabetes. Skeletal muscle glucose uptake can be enhanced by a variety of different stimuli, including insulin and contraction as the most prominent. In contrast to the clearance of glucose from the bloodstream in response to insulin stimulation, exercise-induced glucose uptake into skeletal muscle is unaffected during the progression of insulin resistance, placing physical activity at the center of prevention and treatment of metabolic diseases. The two Rab GTPase-activating proteins (RabGAPs), TBC1D1 and TBC1D4, represent critical nodes at the convergence of insulin- and exercise-stimulated signaling pathways, as phosphorylation of the two closely related signaling factors leads to enhanced translocation of glucose transporter 4 (GLUT4) to the plasma membrane, resulting in increased cellular glucose uptake. However, the full network of intracellular signaling pathways that control exercise-induced glucose uptake and that overlap with the insulin-stimulated pathway upstream of the RabGAPs is not fully understood. In this review, we discuss the current state of knowledge on exercise- and insulin-regulated kinases, hypoxia, nitric oxide (NO) and bioactive lipids that may be involved in the regulation of skeletal muscle glucose uptake.

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Glycyrrhizic Acid Protects Glomerular Podocytes Induced by High Glucose by Modulating SNARK/AMPK Signaling Pathway

Zhao,

Li,

Zhang

et al. 2023

CURR MED SCI

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Sucrose nonfermenting AMPK‐related kinase (SNARK) regulates exercise‐stimulated and ischemia‐stimulated glucose transport in the heart

Cited by 4 publications

References 46 publications

Animal and Cellular Studies Demonstrate Some of the Beneficial Impacts of Herring Milt Hydrolysates on Obesity-Induced Glucose Intolerance and Inflammation

Animal and Cellular Studies Demonstrate Some of the Beneficial Impacts of Herring Milt Hydrolysates on Obesity-Induced Glucose Intolerance and Inflammation

AMPK and Beyond: The Signaling Network Controlling RabGAPs and Contraction-Mediated Glucose Uptake in Skeletal Muscle

Glycyrrhizic Acid Protects Glomerular Podocytes Induced by High Glucose by Modulating SNARK/AMPK Signaling Pathway

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