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

Malnutrition is a common complicating factor in surgical illness. To investigate the cellular changes and mechanisms responsible for the protein wasting associated with nutritional deprivation, Sprague-Dawley rats were subjected to total protein-calorie starvation for 3 (n = 12) or 5 days (n = 12) and compared to freely fed animals monitored for 3 (n = 8) or 5 (n = 8) days. Gastrocnemius protein and RNA content and levels of mRNA coding for the myofibrillar proteins myosin heavy chain, myosin light chain, and alpha-actin were measured. Starvation resulted in a significant decrease in gastrocnemius mass and protein content, and was associated with decreases in mRNA levels for the three myofibrillar proteins assayed. We conclude that changes in mRNA levels for these proteins likely contribute to the loss of peripheral protein which occurs during total nutritional deprivation. In addition, the changes in mRNA levels for these three structural proteins appear to be coordinate, suggesting that transcription of no single myofibrillar protein is rate-limiting in the regulation of skeletal muscle protein content.
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PMID:Starvation leads to decreased levels of mRNA for myofibrillar proteins. 249 68

1. Small-intestinal absorption and permeability were measured in nine patients with malnutrition who were receiving liquid enteral nutrition after different periods of starvation, in five patients receiving enteral nutrition without starvation, in six healthy subjects after starvation for 36 h and in two obese subjects starved for 11 days. 2. Absorption, expressed by the plasma 60 min D-xylose level and the plasma 60 min D-xylose/3-O-methyl-D-glucose ratio, was greatly decreased (P less than 0.001) in the nine patients receiving enteral feeding after starvation, whereas permeability, denoted by the 5 h urinary lactulose/rhamnose ratio, was increased (P less than 0.05). 3. The five patients receiving enteral feeds without prior starvation had normal intestinal absorption and permeability. 4. Starvation of the healthy subjects reduced absorption (P less than 0.05) and this was detectable at 36 h. Permeability, however, was not increased by 36 h starvation. Starvation of the obese subjects also progressively reduced absorption, and this was reversed with refeeding. 5. Changes in intestinal function during enteral feeding are similar to those seen in intestinal diseases. They develop rapidly and are not caused or reversed by liquid enteral feeds. Starvation, before beginning feeding, may explain some of the changes found.
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PMID:Small-intestinal function during enteral feeding and starvation in man. 250 27

Two hypotheses have been postulated as to the pathogenesis of hypogonadotropinemia in anorexia nervosa; one is starvation and weight loss and the other is a psychological factor to influence gonadotropin secretion. Our patient suffered from very rare concurrence of Turner's syndrome and anorexia nervosa and a study of this experiment in nature provided important evidences concerning decreased secretion of gonadotropins in the eating disorder. The patient was diagnosed as Turner's syndrome when she was 6 years old. Her gonadotropin levels were elevated to the castrated ranges (LH 61.8 IU/l; FSH 175.8 IU/l) after 8 years of age. She was noticed to be anorectic at the age of 13 years. Serum levels of the pituitary gonadotropins were lowered (LH 2.9 IU/l; FSH 3.0 IU/l) and their responses to luteinizing hormone-releasing hormone were decreased beneath the normal prepubertal limits. After one year of the anorectic period, she recovered the weight though her gonadotropin levels remained in the very low ranges (LH 2.7 IU/l; FSH 2.5 IU/l). The results suggest that hypogonadism in anorexia nervosa is not solely caused by nutritional deficiency but rather by other factors such as psychological abnormalities.
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PMID:Prolonged suppression of gonadotropin secretion after weight recovery in an anorectic patient with Turner's syndrome: reduced gonadal function in anorexia nervosa is independent in part on nutrition. 251 41

Malnutrition has a direct relationship to complications associated with ineffective wound and fracture healing, inadequate immune responses, decreased tolerance to cancer therapy, muscle weakness, and certain organ dysfunctions (heart and liver). Malnutrition combined with disease, injury, or stress increases the metabolic rate in patients above that of resting. These patients are undergoing an accelerated form of starvation, which is more common than presently recognized in veterinary medicine and may be responsible for the less than optimal responses to proper therapies. Diseased or injured patients unable to digest or absorb nutrients from the gastrointestinal tract require additional medical support in the form of parenteral nutrition. Advances in parenteral solutions, products, and delivery systems make parenteral nutritional support possible in veterinary medicine, although not possible in all small animal practices. Proper patient selection, well-informed clients, dedicated technicians, and knowledgeable veterinarians are all essential in the successful implementation of parenteral nutritional support.
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PMID:Parenteral nutritional support in the small animal patient. 251 12

Malnutrition, as well as malignancy, induces alterations in heart metabolism and performance. Previous studies have implicated adrenergic mechanisms as the cause. The present study was undertaken to investigate if the adenylate cyclase system in the rat heart was affected by malnutrition. Three different animal groups with malnutrition were compared with a control group: rats with acute starvation for 14-96 hours, rats with protein-calorie malnutrition for 2 weeks, and rats with tumors. Stimulation by beta-adrenergic receptors and inhibition by muscarinic receptors of adenylate cyclase activity were not altered by malnutrition. However, conditions used for in vitro adenylate cyclase determinations were, of necessity, not physiological. Neither did the number of beta-adrenergic and muscarinic receptors change. When competition-binding experiments were performed, differences comprising agonist affinity and affinity state distribution were noted among the groups. The myocardial beta-adrenergic receptors formed a reduced number of high-affinity sites in all groups as compared with the control rats. All high-affinity sites displayed a more than 10-fold increase in affinity toward isoproterenol and an impaired sensitivity to guanine nucleotides except in heart membranes derived from rats starved less than 48 hours. While the protein-calorie restricted and the tumor-bearing rats had myocardial beta-adrenergic receptors that were unresponsive to guanine nucleotides, after 48 hours of starvation the rats exhibited an attenuated guanine-nucleotide-induced affinity shift. No changes associated with malnutrition in myocardial membrane levels of the of the stimulatory guanine-nucleotide-binding protein were detected by cholera-toxin-induced ADP-ribosylation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of malnutrition on rat myocardial beta-adrenergic and muscarinic receptors. 253 24

A mutation in the gene IRA1 (formerly called PPD1) was originally characterized as a deficiency of a phosphoprotein phosphatase. The IRA1 gene has been cloned and sequenced. A large open reading frame (8,817 base pairs) which can encode a protein of 2,938 amino acids was found. Northern (RNA) blot analysis detected a message of about 10 kilobases, and nuclease S1 protection demonstrated mRNA start points at 97 and 98 base pairs upstream from the putative initiator ATG codon. Disruption of the IRA1 gene resulted in sensitivity to nitrogen starvation and heat shock. Diploids homozygous for the disrupted IRA1 gene were deficient in sporulation. Disruption of the IRA1 gene suppressed the lethality of the cdc25 mutation but did not suppress the lethality of either the ras1 ras2 or the cyr1 mutations. Deficiency of the phosphoprotein phosphatase was not reproducible in the disruption mutant of the IRA1 gene. Moreover, the ira1 mutant showed an increased level of cyclic AMP. Our results suggest that the IRA1 protein inhibits the function of the RAS proteins in a fashion antagonistic to the function of the CDC25 protein in the RAS-cyclic AMP pathway in Saccharomyces cerevisiae.
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PMID:IRA1, an inhibitory regulator of the RAS-cyclic AMP pathway in Saccharomyces cerevisiae. 254 Apr 26

The respiratory properties of isolated rat renal mitochondria after fasting conditions (2-8 days) are estimated in comparison with the parameters of normal feeded control animals. After an extrem starvation time of 8 days the active and uncoupled respiration of glutamate/malate, but not of succinate were reduced, whereas the respiratory control index and the ADP/O-Quotient did remain unchanged. In conclusion, malnutrition do not influence the renal function due to mitochondrial changes.
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PMID:[Functional properties of isolated kidney mitochondria of rats in food deprivation]. 256 21

The 5 alpha-reductase, the enzyme which converts testosterone into its major "active" metabolite (dihydrotestosterone, DHT), has been found to be present in high concentration in brain structures particularly rich of myelin (white matter structures), as well as in myelin membranes. Previous ontogenetic observations seem to indicate that, during the process of myelinogenesis, the enzyme might be synthesized in the oligodendrocytes, and subsequently incorporated into the myelin membranes. It is well established that postnatal malnutrition produces a decreased formation of myelin, when starvation is performed from birth until to the 2nd or 3rd week of life; on the contrary food deprivation does not produce any significant effect on myelin accumulation when performed after the 14th day of life. The present experiments have been performed in the rat in order to study the effects of postnatal undernutrition (from birth to the 19th day of life: long malnutrition; and from the 14th to the 19th day of life: short malnutrition) on the 5 alpha-reductase activity present in the following brain structures: cerebral cortex, hypothalamus, corpus callosum, pyramidal tract, as well as in isolated myelin membranes. Undernourished animals have been killed at 20 days of age. Normally nourished animals served as controls. Long undernutrition induced a statistically significant decrease of the formation of DHT in the corpus callosum and in the pyramidal tract vs controls. On the contrary, the nutritional deficiency did not decrease the 5 alpha-reductase activity in the cerebral cortex and in the hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of postnatal starvation on the 5 alpha-reductase activity of the brain and of the isolated myelin membranes. 263 Mar 7

During the past decade, Africa, more than any other continent, has been associated with famine and malnutrition. The Sahelian drought of the early 1970s, the Wollo and Karamoja famines and most recently, mass starvation in Ethiopia, have followed one another in rapid succession. The term 'food crisis' continually crops up in the popular and academic press. An increasing number of researchers probe possible causes; many seek a systemic reason for the present situation. One working hypothesis is that increasing commoditization of food has undermined Africa's food systems. This paper does not purport to prove or disprove this. Less ambitiously, its aim is to draw attention to inter-relationships between commoditization and physical and social aspects of African food systems, tracing their possible effects on the nutritional status of the African population. In so doing, some of the complexities of developing food production and consumption in the transition from peasant societies to more urban-based national economies become evident. The paper is divided into three main parts: a discussion of conceptual categories and general background information about sub-Saharan African food zones and commodity and factor markets; a review of literature on rural food availability and nutrition; and a review of urban food availability and nutrition.
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PMID:Nutrition and the commoditization of food in sub-Saharan Africa. 264 97

Anorexia nervosa is a common psychiatric disorder predominantly affecting young women, associated with significant morbidity and mortality, much involving the cardiovascular system. In contrast, protein-calorie malnutrition, while not strictly analogous to the protein-sparing characteristics often noted in anorexia nervosa, is a problem of global stature. Physiologic consequences of anorexia nervosa include rhythm disturbances, mitral valve prolapse, plus both systolic and diastolic ventricular dysfunction. Diminished exercise capacity occurs in both states, with marked blunting of the heart rate and blood pressure response. Congestive heart failure may appear, especially during refeeding. In addition to the myofibrillar destruction associated with protein-calorie malnutrition, hypophosphatemia, particularly when exacerbated by unrestricted glucose-rich refeedings or hyperalimentation, may be one additional cause of ventricular dysfunction. A high level of suspicion for cardiovascular complications is, therefore, warranted in the evaluation and therapy of weight loss conditions such as starvation and anorexia nervosa.
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PMID:Weight loss and the heart. Effects of anorexia nervosa and starvation. 265 Jun 47


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