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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spinal muscular atrophy (SMA) is a genetic neuromuscular disease characterized by progressive muscle weakness and atrophy. We report a case of a 36-year-old man with SMA type 3 who presented to our emergency department with epigastric pain and vomiting. He was found to have severe ketoacidosis on laboratory evaluation. The patient's symptoms and ketoacidosis resolved after dextrose infusion and a relatively small amount of sodium bicarbonate infusion. Given the severity of the ketosis that seemed inconsistent with moderate starvation alone, we postulate that there must have been other contributing factors besides moderate starvation that might explain the severity of acidosis in this particular patient. These factors include low muscle mass, disturbed fatty acid metabolism, hormonal imbalances and defective glucose metabolism. Ketoacidosis is an under-recognized entity in patients with neuromuscular diseases and requires a high index of suspicion for prompt diagnosis and management.
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PMID:Severe ketoacidosis in a patient with spinal muscular atrophy. 2997 96

A 49-year-old lady with no past medical history presented with dysphagia and 40-pound weight loss, which occurred over eight months. On physical examination, she had proximal muscle weakness and crackles in basilar regions of the lungs. Labs were significant for low albumin, elevated transaminases, and high aldolase. Imaging suggested aspiration pneumonitis in both lungs and hepatic steatosis. A swallow evaluation revealed oropharyngeal dysphagia and muscle biopsy confirmed a rare form of myositis. A liver biopsy showed steatohepatitis and a diagnosis of starvation-induced steatohepatitis was made. The patient succumbed to hypoxic respiratory failure from aspiration pneumonitis before the treatment for myositis could be initiated. We report the first case of starvation-induced steatohepatitis in a patient with dysphagia from myositis affecting the oropharyngeal musculature.
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PMID:Thin Patient, Fatty Liver. 3105 22

Severely undernourished and underweight anorexia nervosa (AN) patients typically remain active and mobile. Might such persistent physical activity in AN be supported by specific adaptations in muscle tissue during long term undernutrition? To identify potential differences, studies examining the effects of undernutrition on skeletal muscle mass, muscle morphology and muscle function in healthy humans and in AN patients were reviewed. Adjustments in muscle morphology and function in AN did not differ in substance from those in healthy humans, undernourished people, or undergoing semi-starvation. Loss of muscle mass, changes in muscle contractility and atrophy of muscle fibers (predominantly type II fibers) characterized both groups. Muscle innervation was unaffected. Work capacity in men in semi-starvation experiments and in females with AN declined by about 70% and 50%, respectively. Perceptions of fatigue and effort distinguished the groups: signs of general weakness, tiring quickly and avoidance of physical activity that were recorded in semi-starvation were not reported for AN patients. The absence of distinctive starvation-related adjustments in skeletal muscle in AN suggests that new methods, such as muscle gene expression profiles in response to deficient nutrient intake, and better knowledge of the central regulatory circuitries contributing to motor urgency will be required to shed light on the persistent mobility in AN patients.
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PMID:Might Starvation-Induced Adaptations in Muscle Mass, Muscle Morphology and Muscle Function Contribute to the Increased Urge for Movement and to Spontaneous Physical Activity in Anorexia Nervosa? 3266 48

Cancer cells have high demands for non-essential amino acids (NEAAs), which are precursors for anabolic and antioxidant pathways that support cell survival and proliferation. It is well-established that cancer cells consume the NEAA cysteine, and that cysteine deprivation can induce cell death; however, the specific factors governing acute sensitivity to cysteine starvation are poorly characterized. Here, we show that that neither expression of enzymes for cysteine synthesis nor availability of the primary precursor methionine correlated with acute sensitivity to cysteine starvation. We observed a strong correlation between efflux of the methionine-derived metabolite methylthioadenosine (MTA) and sensitivity to cysteine starvation. MTA efflux results from genetic deletion of methylthioadenosine phosphorylase (MTAP), which is frequently deleted in cancers. We show that MTAP loss upregulates polyamine metabolism which, concurrently with cysteine withdrawal, promotes elevated reactive oxygen species and prevents cell survival. Our results reveal an unexplored metabolic weakness at the intersection of polyamine and cysteine metabolism.
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PMID:Polyamine pathway activity promotes cysteine essentiality in cancer cells. 3274 94


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