Protein-Energy Malnutrition Causes Deficits in Motor Function in Adult Male Rats

Alaverdashvili, Mariam; Li, Xue; Paterson, Phyllis G.

doi:10.3945/jn.115.216382

Cited by 19 publications

(12 citation statements)

References 55 publications

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“…The loss of muscle mass and decreased cross‐sectional area in the plantaris muscle were observed in the malnutrition group, but no atrophy was observed in the soleus muscle. Several previous studies reported that excessive dietary restriction or ingestion of a low‐protein diet results in loss of muscle mass in fast muscles (Kim, 2013; Pereyra‐Venegas et al, 2015; Ruiz‐Rosado et al, 2013; Toyoshima et al, 2014) and no atrophy was induced in slow muscles (Alaverdashvili et al, 2015; Salles et al, 2014; Walrand et al, 2000). In addition, Sakaida et al, (1987) reported that glycogen content in muscle fibers decreased predominantly in type IIB fibers after 2 days of starvation and almost disappeared after 4 days.…”

Section: Discussionmentioning

confidence: 99%

Reduced metabolic capacity in fast and slow skeletal muscle via oxidative stress and the energy‐sensing of AMPK/SIRT1 in malnutrition

et al. 2021

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The effects of malnutrition on skeletal muscle result in not only the loss of muscle mass but also fatigue intolerance. It remains unknown whether the metabolic capacity is related to the fiber type composition of skeletal muscle under malnourished condition although malnutrition resulted in preferential atrophy in fast muscle. The purpose of the present study was to investigate the effects of metabolic capacity in fast and slow muscles via the energy‐sensing of AMPK and SIRT1 in malnutrition. Wistar rats were randomly divided into control and malnutrition groups. The rats in the malnutrition group were provided with a low‐protein diet, and daily food intake was limited to 50% for 12 weeks. Malnutrition with hypoalbuminemia decreased the body weight and induced the loss of plantaris muscle mass, but there was little change in the soleus muscle. An increase in the superoxide level in the plasma and a decrease in SOD‐2 protein expression in both muscles were observed in the malnutrition group. In addition, the expression level of AMPK in the malnutrition group increased in both muscles. Conversely, the expression level of SIRT1 decreased in both muscles of the malnutrition group. In addition, malnutrition resulted in a decrease in the expression levels of PGC‐1α and PINK protein, and induced a decrease in the levels of two key mitochondrial enzymes (succinate dehydrogenase and citrate synthase) and COX IV protein expression in both muscles. These results indicate that malnutrition impaired the metabolic capacity in both fast and slow muscles via AMPK‐independent SIRT1 inhibition induced by increased oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Reduced metabolic capacity in fast and slow skeletal muscle via oxidative stress and the energy‐sensing of AMPK/SIRT1 in malnutrition

et al. 2021

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“…Previous studies in animal models of focal cerebral ischemia found that undernutrition reduces brain injury [7-9, 16, 17], whereas other studies in models of focal or global ischemia showed that ischemic injury was unchanged by undernutrition [10][11][12][13]. A variety of studies in models of focal or global ischemia observed a significant reduction of stroke-induced neurological deficits [7][8][9][10][11], whereas other studies, again in focal or global ischemia, noted exacerbated or unchanged deficits [12][13][14][15]. Major differences in these studies relate to the type of undernutrition.…”

Section: Discussionmentioning

confidence: 99%

“…Major differences in these studies relate to the type of undernutrition. As such, undernutrition was induced by (a) reducing food access to 60 or 70% of the average amount of control animals for 4 weeks to 3 months [8,10,13,16], (b) reducing food protein content to 0 to 12% for 6 days to 4 weeks [9,12,14,15], or (c) intermittent fasting on alternate days or twice per week for one to several months [7,11,17]. While reducing the amount of food access similarly reduces protein and energy consumption, the reduction of protein content to 0-2% results in a reduction in the total amount of food ingested, since the animals refuse this chow [9,12,14,15].…”

Section: Discussionmentioning

confidence: 99%

“…Electronic supplementary material The online version of this article (https://doi.org/10.1007/s12975-019-00700-3) contains supplementary material, which is available to authorized users. experimental studies showed that continuous or intermittent food restriction reduces post-ischemic neurological deficits [7][8][9][10][11], whereas other studies found exacerbated or unchanged neurological impairments [12][13][14][15]. Some studies showed that undernutrition reduced histological brain injury [7-9, 16, 17], whereas other studies observed no effect [10][11][12][13].…”

Section: Introductionmentioning

confidence: 99%

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Neuroprotection Induced by Energy and Protein-Energy Undernutrition Is Phase-Dependent After Focal Cerebral Ischemia in Mice

Carvalho

Sánchez-Mendoza

Melo

et al. 2019

Transl. Stroke Res.

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Malnutrition predisposes to poor stroke outcome. In animal models, undernutrition protected against ischemic injury in some, but not in other studies. In view of diverse stroke models and food restriction paradigms, the consequences of undernutrition are poorly understood. Herein, we exposed mice to energy-reduced and protein-energy-reduced diets for 7-30 days and subsequently induced intraluminal middle cerebral artery occlusion. Undernutrition phase dependently influenced ischemic injury. Shortlasting 7 days of protein-energy undernutrition, but not energy undernutrition, decreased post-ischemic brain leukocyte infiltration and microglial activation and reduced brain Il-1β mRNA, but did not protect against ischemic injury. Fourteen days of energy and protein-energy undernutrition, on the other hand, reduced ischemic injury despite absence of anti-inflammatory effects. Anti-oxidant genes (Sod-1, Sod-2, and Cat mRNAs) were regulated in the liver and, to a lesser extent, the ischemic brain, indicating an adapted, compensated stage. Conversely, 30 days of energy and protein-energy undernutrition caused progressive animal exhaustion associated with post-ischemic hypoperfusion, rise of metabolic markers (Sirt-1 and Glut-1 mRNAs, Sirt-1 protein) in the ischemic brain, and reregulation of pro-and anti-oxidant markers (now also Nox-4 and Gpx-3 mRNAs) in the liver. In the latter condition, no neuroprotection was noted. Our study suggests an adaptation of metabolic systems that provides neuroprotection in a circumscribed time window.

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“…23 These effects of PEM on cardiac function caused by muscle atrophy are due to inadequate protein and cardiovascular energy or indirectly due to metabolic disorders and increased systemic demand. 24…”

Section: Discussionmentioning

confidence: 99%

Study of NT-pro-BNP and Hs-Troponin I Biomarkers for Early Detection of Children’s Heart Function of Protein-Energy Malnutrition

et al. 2019

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The Protein Energy Malnutrition (PEM) is the condition of a lack of carbohydrate and protein stores in the body that trigger chronic failure nutrient intake and body maintenance function caused to impact the heart functions. The NT-pro-BNP and Hs- Troponin I proteins were found as the indicator of cardiac dysfunction. The sixty subjects of PEM, analyzed by standard of Indonesia Healt Ministry as well as nutritional status. The blood electrolytes examined by laboratory assay and the levels of Hs-Troponin 1 and NT-Pro-BNP were analyzed by Immune-Chromatography method. Assessing of the ventricular mass with the seeing the peak of the diastolic flow rate of left ventricular that estimated by the curve of the receiver operating characteristic and the area under the curve (P<0.05). The result has shown that the PEM decreased in the left ventricular mass for impaired heart function and systolic disorder. The Hs- Troponin I (90.9%) has better sensitivity than NT-pro-BNP (85.5%) if the merger of those markers possesses the lowest sensitivity (81.8%). These proteins have good biomarkers in heart function, mainly in cases where PEM is present.

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Protein-Energy Malnutrition Causes Deficits in Motor Function in Adult Male Rats

Cited by 19 publications

References 55 publications

Reduced metabolic capacity in fast and slow skeletal muscle via oxidative stress and the energy‐sensing of AMPK/SIRT1 in malnutrition

Reduced metabolic capacity in fast and slow skeletal muscle via oxidative stress and the energy‐sensing of AMPK/SIRT1 in malnutrition

Neuroprotection Induced by Energy and Protein-Energy Undernutrition Is Phase-Dependent After Focal Cerebral Ischemia in Mice

Study of NT-pro-BNP and Hs-Troponin I Biomarkers for Early Detection of Children’s Heart Function of Protein-Energy Malnutrition

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