Effect of a Low-Protein Diet Supplemented with Ketoacids on Skeletal Muscle Atrophy and Autophagy in Rats with Type 2 Diabetic Nephropathy

Huang, Juan; Wang, Jialin; Gu, Leyi; Bao, Jinsong; Yin, Jun; Tang, Zefan; Wang, Ling; Wang, Yuan

doi:10.1371/journal.pone.0081464

Cited by 13 publications

(14 citation statements)

References 60 publications

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“…This nerve disorder causes indeed motor dysfunction leading to muscle weakness and atrophy [ 61 – 63 ]. Diabetic neuropathy could further, in combination to increased autophagy already reported in this model [ 64 ], explains the smaller size of gastrocnemius muscle we reported herein.…”

Section: Discussionsupporting

confidence: 76%

Insulin Resistance Is Not Associated with an Impaired Mitochondrial Function in Contracting Gastrocnemius Muscle of Goto-Kakizaki Diabetic Rats In Vivo

et al. 2015

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Insulin resistance, altered lipid metabolism and mitochondrial dysfunction in skeletal muscle would play a major role in type 2 diabetes mellitus (T2DM) development, but the causal relationships between these events remain conflicting. To clarify this issue, gastrocnemius muscle function and energetics were investigated throughout a multidisciplinary approach combining in vivo and in vitro measurements in Goto-Kakizaki (GK) rats, a non-obese T2DM model developing peripheral insulin resistant without abnormal level of plasma non-esterified fatty acids (NEFA). Wistar rats were used as controls. Mechanical performance and energy metabolism were assessed strictly non-invasively using magnetic resonance (MR) imaging and 31-phosphorus MR spectroscopy (31P-MRS). Compared with control group, plasma insulin and glucose were respectively lower and higher in GK rats, but plasma NEFA level was normal. In resting GK muscle, phosphocreatine content was reduced whereas glucose content and intracellular pH were both higher. However, there were not differences between both groups for basal oxidative ATP synthesis rate, citrate synthase activity, and intramyocellular contents for lipids, glycogen, ATP and ADP (an important in vivo mitochondrial regulator). During a standardized fatiguing protocol (6 min of maximal repeated isometric contractions electrically induced at a frequency of 1.7 Hz), mechanical performance and glycolytic ATP production rate were reduced in diabetic animals whereas oxidative ATP production rate, maximal mitochondrial capacity and ATP cost of contraction were not changed. These findings provide in vivo evidence that insulin resistance is not caused by an impairment of mitochondrial function in this diabetic model.

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Section: Discussionsupporting

confidence: 76%

Insulin Resistance Is Not Associated with an Impaired Mitochondrial Function in Contracting Gastrocnemius Muscle of Goto-Kakizaki Diabetic Rats In Vivo

et al. 2015

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“…Diabetic GK rats also present a reduction in muscle mass and a decreased muscle fiber size [157]. Under these conditions, the expression of autophagic genes and the abundance of autophagosomes are increased in the muscle of these animals [157].…”

Section: Rodent Models Of Type 2 Diabetes Mellitusmentioning

confidence: 99%

“…Under these conditions, the expression of autophagic genes and the abundance of autophagosomes are increased in the muscle of these animals [157]. D. Sala, A. Zorzano In contrast to most models of type 2 diabetes, obesity induced by a high-fat diet for 14 weeks does not alter muscle mass in mice (Table 1) [158].…”

Section: Rodent Models Of Type 2 Diabetes Mellitusmentioning

confidence: 99%

Differential control of muscle mass in type 1 and type 2 diabetes mellitus

Sala

Zorzano

2015

Cell. Mol. Life Sci.

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Diabetes mellitus--whether driven by insulin deficiency or insulin resistance--causes major alterations in muscle metabolism. These alterations have an impact on nutrient handling, including the metabolism of glucose, lipids, and amino acids, and also on muscle mass and strength. However, the ways in which the distinct forms of diabetes affect muscle mass differ greatly. The most common forms of diabetes mellitus are type 1 and type 2. Thus, whereas type 1 diabetic subjects without insulin treatment display a dramatic loss of muscle, most type 2 diabetic subjects show no changes or even an increase in muscle mass. However, the most commonly used rodent models of type 2 diabetes are characterized by muscle atrophy and do not mimic the features of the disease in humans in terms of muscle mass. In this review, we analyze the processes that are differentially regulated under these forms of diabetes and propose regulatory mechanisms to explain them.

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“…), and Huang et al . () observed similar structures in the soleus muscles of rats with type 2 diabetic nephropathy in a low‐protein diet model. The so‐called myelin figures are reeled membranous structures consisting of phospholipids that can substitute for a cluster of dead cells.…”

Section: Discussionmentioning

confidence: 65%

Neuromuscular junctions (NMJs): ultrastructural analysis and nicotinic acetylcholine receptor (nAChR) subunit mRNA expression in offspring subjected to protein restriction throughout pregnancy

Castro¹,

Faccioni

Bôer

et al. 2017

Int J Experimental Path

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Protein restriction during gestation can alter the skeletal muscle phenotype of offspring; however, little is known with regard to whether this also affects the neuromuscular junction (NMJ), as muscle phenotype maintenance depends upon NMJ functional integrity. This study aimed to evaluate the effects of a low protein (6%) intake by dams throughout gestation on male offspring NMJ morphology and nicotinic acetylcholine receptor (nAChR) α1, γ and ε subunit expression in the soleus (SOL) and extensor digitorum longus (EDL) muscles. Four groups of male Wistar offspring rats were studied. The offspring of dams fed low-protein (6% protein, LP) and normal protein (17% protein, NP) diets were evaluated at 30 and 120 days of age, and the SOL and EDL muscles were collected for analysis. Morphological studies using transmission electron microscopy revealed that only SOL NMJs were affected in 30-day-old offspring in the LP group compared with the NP group. SOL NMJs exhibited fewer synaptic folds, the postsynaptic membranes were smooth and myelin figures were also frequently observed in the terminal axons. With regard to the expression of mRNAs encoding nAChR subunits, only 30-day-old LP offspring EDL muscles exhibited reduced α, γ and ε subunit expression compared with the NP group. In conclusion, our results demonstrate that a low-protein diet (6%) imposed throughout pregnancy impairs the expression of mRNAs encoding the nAChR α, γ and ε subunits in EDL NMJs and promotes morphological changes in SOL NMJs of 30-day-old offspring, indicating specific differences among muscle types following long-term maternal protein restriction.

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Effect of a Low-Protein Diet Supplemented with Ketoacids on Skeletal Muscle Atrophy and Autophagy in Rats with Type 2 Diabetic Nephropathy

Cited by 13 publications

References 60 publications

Insulin Resistance Is Not Associated with an Impaired Mitochondrial Function in Contracting Gastrocnemius Muscle of Goto-Kakizaki Diabetic Rats In Vivo

Insulin Resistance Is Not Associated with an Impaired Mitochondrial Function in Contracting Gastrocnemius Muscle of Goto-Kakizaki Diabetic Rats In Vivo

Differential control of muscle mass in type 1 and type 2 diabetes mellitus

Neuromuscular junctions (NMJs): ultrastructural analysis and nicotinic acetylcholine receptor (nAChR) subunit mRNA expression in offspring subjected to protein restriction throughout pregnancy

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