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The effects of diet composition and chronic obesity on muscle growth and function.
Sousa, Luís G O de; Marshall, Andrea G; Norman, Jennifer E; Fuqua, Jordan D; Lira, Vitor A; Rutledge, John C; Bodine, Sue C.
Afiliação
  • Sousa LGO; Division of Endocrinology and Metabolism, Department of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa.
  • Marshall AG; Division of Endocrinology and Metabolism, Department of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa.
  • Norman JE; Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, California.
  • Fuqua JD; Department of Health and Human Physiology, Obesity Research and Education Initiative, Fraternal Order of Eagles (F.O.E.) Diabetes Research Center, Abboud Cardiovascular Research Center, Pappajohn Biomedical Institute, The University of Iowa, Iowa City, Iowa.
  • Lira VA; Department of Health and Human Physiology, Obesity Research and Education Initiative, Fraternal Order of Eagles (F.O.E.) Diabetes Research Center, Abboud Cardiovascular Research Center, Pappajohn Biomedical Institute, The University of Iowa, Iowa City, Iowa.
  • Rutledge JC; Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, California.
  • Bodine SC; Division of Endocrinology and Metabolism, Department of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa.
J Appl Physiol (1985) ; 130(1): 124-138, 2021 01 01.
Article em En | MEDLINE | ID: mdl-33211595
ABSTRACT
Diet-induced obesity (DIO) is associated with glucose intolerance, insulin resistance (IR), and an increase in intramyocellular lipids (IMCL), which may lead to disturbances in glucose and protein metabolism. To this matter, it has been speculated that chronic obesity and elevated IMCL may contribute to skeletal muscle loss and deficits in muscle function and growth capacity. Thus, we hypothesized that diets with elevated fat content would induce obesity and insulin resistance, leading to a decrease in muscle mass and an attenuated growth response to increased external loading in adult male mice. Male C57BL/6 mice (8 wk of age) were subjected to five different diets, namely, chow, low-dat-diet (LFD), high-fat-diet (HFD), sucrose, or Western diet, for 28 wk. At 25 wk, HFD and Western diets induced a 60.4% and 35.9% increase in body weight, respectively. Interestingly, HFD, but not Western or sucrose, induced glucose intolerance and insulin resistance. Measurement of isometric torque (ankle plantar flexor and ankle dorsiflexor muscles) revealed no effect of DIO on muscle function. At 28 wk of intervention, muscle area and protein synthesis were similar across all diet groups, despite insulin resistance and increased IMCL being observed in HFD and Western diet groups. In response to 30 days of functional overload, an attenuated growth response was observed in only the HFD group. Nevertheless, our results show that DIO alone is not sufficient to induce muscle atrophy and contractile dysfunction in adult male C57BL/6 mice. However, diet composition does have an impact on muscle growth in response to increased external loading.NEW & NOTEWORTHY The effects of diet-induced obesity on skeletal muscle mass are complex and dependent on diet composition and diet duration. The present study results show that chronic exposure to high levels of fatty acids does not affect muscle mass, contractile function, or protein synthesis in obese C57BL/6 mice compared with the consumption of chow. Obesity did result in a delay in load-induced growth; however, only a 45% HFD resulted in attenuated growth following 30 days of functional overload.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Resistência à Insulina / Intolerância à Glucose Limite: Animals Idioma: En Ano de publicação: 2021 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Resistência à Insulina / Intolerância à Glucose Limite: Animals Idioma: En Ano de publicação: 2021 Tipo de documento: Article