Impaired glucose metabolism and exercise capacity with muscle-specific glycogen synthase 1 (gys1) deletion in adult mice

Xirouchaki, Chrysovalantou E.; Mangiafico, Salvatore; Bate, Katherine; Ruan, Zheng; Huang, Mengjie; Tedjosiswoyo, Bing Wilari; Lamont, Benjamin J.; Pong, W.Y.; Favaloro, Jenny M.; Blair, Amy R.; Zajac, Jeffrey D; Proietto, Joseph; Andrikopoulos, Sofianos

doi:10.1016/j.molmet.2016.01.004

Cited by 58 publications

(42 citation statements)

References 70 publications

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“…Skeletal muscle metabolism is critical to maintain fuel homeostasis during exercise. In both male rats and mice, androgen deficiency decreases muscle glycogen stores (Ramamani et al 1999, Dubois et al 2016, a suggested risk factor for fatigue development (Xirouchaki et al 2016). Conversely, testosterone promotes glucose uptake in skeletal muscle, although it is not clear to what extent these effects are dependent on local AR actions (Sato et al 2008, Ibebunjo et al 2011, Dubois et al 2016, Kelly et al 2016.…”

Section: Other Peripheral Actionsmentioning

confidence: 99%

Androgen and estrogen actions on male physical activity: a story beyond muscle

Jardí

Laurent

Dubois

et al. 2018

Journal of Endocrinology

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Physical inactivity is a pandemic that contributes to several chronic diseases and poses a significant burden on health care systems worldwide. The search for effective strategies to combat sedentary behavior has led to an intensification of the research efforts to unravel the biological substrate controlling activity. A wide body of preclinical evidence makes a strong case for sex steroids regulating physical activity in both genders, albeit the mechanisms implicated remain unclear. The beneficial effects of androgens on muscle as well as on other peripheral functions might play a role in favoring adaptation to exercise. Alternatively or in addition, sex steroids could act on specific brain circuitries to boost physical activity. This review critically discusses the evidence supporting a role for androgens and estrogens stimulating male physical activity, with special emphasis on the possible role of peripheral and/or central mechanisms. Finally, the potential translation of these findings to humans is briefly discussed.

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Section: Other Peripheral Actionsmentioning

confidence: 99%

Androgen and estrogen actions on male physical activity: a story beyond muscle

Jardí

Laurent

Dubois

et al. 2018

Journal of Endocrinology

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“…Glycogen synthesis is a major fate for glucose uptake in the body, and glycogen synthase is a key enzyme related to whole-body insulin sensitivity. Previous studies have shown impaired glucose tolerance and metabolism in liver or muscle glycogen synthase knock-out mice [15,16]. Therefore, we speculate that suppressing the insulin signal pathway in liver and muscle may lead to a reduction in glucose utilization, thus impairing the glucose tolerance in the offspring under maternal HE diet treatment.…”

Section: Discussionmentioning

confidence: 73%

Dietary Energy Levels from Middle to Late Gestation of Guangdong Small-Ear Spotted Pig: Effects on Body Weight, Muscle Development, and Glucose Metabolism of its Newborn Piglets

Yang

Chen

et al. 2020

Preprint

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Background: Guangdong Small-ear Spotted pigs are Chinese indigenous pig that have the characteristic of desired meat quality and resistance to coarse feeding. However, no study has elucidated the effects of dietary energy levels on body weight, muscle development and glucose metabolism of its newborn piglets. Therefore, a total of 66 pregnant gilts with an average body weight of 80.6±6.6 kg at day 60 of gestation were randomly divided into two groups: control group (CON group; 11.50 MJ/kg digestible energy), and high-energy diet group (HE group; 13.42 MJ/kg digestible energy). Results: The results showed that the maternal HE diet was shown to decrease the birth weight of piglets that from the gilts with total or alive litter size of 12 to 13. Additionally, the HE diet group were shown to impair the glucose tolerance of newborn piglets, as evidenced by the glucose tolerance test and the inhibition of insulin signaling pathway in liver and soleus muscle. Despite no significant change in the muscle weight in the two groups, the maternal HE diet was shown to downregulate the protein level of slow-twitch fiber myosin heavy chain I (MyHC I), and upregulate the protein levels of fast-twitch fiber myosin heavy chain IIb (MyHC IIb) and IIx (MyHC IIx) in soleus muscle of their progeny. Furthermore, the newborn piglets in HE group were showed a decrease in mitochondrial biogenesis in liver and soleus muscle when compared to that in CON group. Conclusions: Maternal high-energy diet from middle to late gestation decreases the birth weight of piglets that from the gilts with total or alive litter size of 12 to 13, induces the formation of glycolytic muscle fibers, and impairs glucose tolerance of their newborn piglets.

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“…Hyperinsulinemic–euglycemic clamps were performed as previously described in 6-hour–fasted mice. 26 An initial 2-minute priming dose of insulin (150 mU/kg/min) was followed by constant infusion at a rate of 15 mU/kg/min. Maintenance of euglycemia was achieved by a variable infusion of 25% glucose solution.…”

Section: Methodsmentioning

confidence: 99%

Ferroportin Expression in Adipocytes Does Not Contribute to Iron Homeostasis or Metabolic Responses to a High Calorie Diet

Britton

Jaskowski

Bridle

et al. 2018

Cellular and Molecular Gastroenterology and Hepatology

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Background & AimsIron has an increasingly recognized role in the regulation of adipose tissue function, including the expression of adipokines involved in the pathogenesis of nonalcoholic fatty liver disease. The cellular iron exporter, ferroportin, has been proposed as being a key determinant of adipocyte iron homeostasis.MethodsWe studied an adipocyte-specific ferroportin (Fpn1) knockout mouse model, using an Adipoq-Cre recombinase driven Fpn1 deletion and fed mice according to the fast food diet model of nonalcoholic steatohepatitis.ResultsWe showed successful selective deletion of Fpn1 in adipocytes, but found that this did not lead to increased adipocyte iron stores as measured by atomic absorption spectroscopy or histologically quantified iron granules after staining with 3,3’-diaminobenzidine–enhanced Perls’ stain. Mice with adipocyte-specific Fpn1 deletion did not show dysregulation of adiponectin, leptin, resistin, or retinol-binding protein-4 expression. Similarly, adipocyte-specific Fpn1 deletion did not affect insulin sensitivity during hyperinsulinemic–euglycemic clamp studies or lead to histologic evidence of increased liver injury. We have shown, however, that the fast food diet model of nonalcoholic steatohepatitis generates an increase in adipose tissue macrophage infiltration with crown-like structures, as seen in human beings, further validating the utility of this model.ConclusionsFerroportin may not be a key determinant of adipocyte iron homeostasis in this knockout model. Further studies are needed to determine the mechanisms of iron metabolism in adipocytes and adipose tissue.

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Impaired glucose metabolism and exercise capacity with muscle-specific glycogen synthase 1 (gys1) deletion in adult mice

Cited by 58 publications

References 70 publications

Androgen and estrogen actions on male physical activity: a story beyond muscle

Androgen and estrogen actions on male physical activity: a story beyond muscle

Dietary Energy Levels from Middle to Late Gestation of Guangdong Small-Ear Spotted Pig: Effects on Body Weight, Muscle Development, and Glucose Metabolism of its Newborn Piglets

Ferroportin Expression in Adipocytes Does Not Contribute to Iron Homeostasis or Metabolic Responses to a High Calorie Diet

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