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

To evaluate the effect ketone bodies on protein metabolism beta-hydroxybutyrate was infused into healthy nonobese and obese subjects and insulin dependent diabetics in the postabsorptive state and into obese subjects after 3 days and 3-10 wks of starvation. In association with blood ketone increments of 1-2 mM, plasma alanine fell by 25-35% in all treatment groups. Furthermore, the hypoalaninemic effect of beta-hydroxybutyrate was equally demonstrable in fasted subjects, in whom alanine was already reduced. In association with repeated 12 hr infusions of beta-hydroxybutyrate in subjects fasted 5-10 wks, urinary nitrogen fell by 30%, returning to baseline after cessation of the infusions and paralleling the changes in plasma alanine. When endogenous ketonemia was produced by isocaloric carbohydrate restriction (less than 25 gm/day), protein ingestion was associated with a 40-50% greater increase in plasma branched chain amino acids as well as a reduced rise in plasma insulin. The enhanced rise in branched chain amino acids was attributable to decreased net utilization since intravenous leucine also produced a 40% greater elevation in plasma leucine after carbohydrate restriction. When nitrogen balance was compared during hypocaloric (400 Kcal) feeding of a pure protein diet and a mixed diet containing 50% protein and 50% carbohydrate, no significant differences were observed. Isocaloric replacement with carbohydrate failed to accentuate nitrogen wasting, despite a marked lowering of blood and urinary ketones. Our findings support the possibility that ketone bodies contribute to the reduction in proteolysis and decrease in muscle alanine release which characterizes prolonged starvation. However, when endogenous hyperketonemia is induced by carbohydrate restriction, plasma insulin declines and the disposal of ingested protein is impaired. Furthermore, the addition of carbohydrate during hypocaloric feeding reduces hyperketonemia, but does not enhance negative nitrogen balance. These observations suggest that dietary carbohydrate and insulin also promote nitrogen retention and that ketogenic, high protein diets do not confer a unique protein sparing advantage.
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PMID:The effect of ketone bodies and dietary carbohydrate intake on protein metabolism. 694 62

Over the last ten years a large body of information has accumulated which indicates that physiologic changes in the plasma insulin concentration are capable of affecting electrolyte transport by the kidney as well as by variety of other tissues. In the present discussion the effect of insulin on the renal handling of sodium, potassium, phosphate, and calcium is reviewed, with an emphasis on sodium transport (Table 1). An attempt is made to relate the effects of insulin on sodium metabolism to four common clinical situations: (a) hypertension and obesity, (b) sodium wasting in diabetes mellitus, (c) natriuresis of starvation, and (d) sodium retention and edema following refeeding.
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PMID:Insulin and renal sodium handling: clinical implications. 701 90

Data are discussed which demonstrate that insulin plays an important role in sodium metabolism. The primary action of insulin on sodium balance is exerted on the kidney. Increases in plasma insulin concentration within the physiological range stimulate sodium reabsorption by the distal nephron segments and this effect is independent of changes in circulating metabolites or other hormones. Several clinical situations are reviewed: sodium wasting in poorly controlled diabetics, natriuresis of starvation, anti-natriuresis of refeeding and hypertension of obesity, in which insulin-mediated changes in sodium balance have been shown to play an important pathophysiological role.
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PMID:The effect of insulin on renal sodium metabolism. A review with clinical implications. 702 50

We measured the effects of seven consecutive daily infusions of alpha-ketoisocaproate (the alpha-keto analogue of leucine) or leucine itself on urinary urea and total nitrogen excretion during fasting. Two study protocols were undertaken. In protocol I, subjects underwent three separate 14-d fasts: one during which 34 mmol/d of leucine were infused on days 1--7; a second during which 34 mmol/d of alpha-ketoisocaproate were infused on days 1--7; and a third control fast during which no infusions were given. Infusions of alpha-ketoisocaproate significantly reduced daily urine urea nitrogen excretion compared with both the control fasts and the fasts in which leucine was infused (P less than 0.001). This nitrogen-sparing effect of alpha-ketoisocaproate persisted during days 8--14 even though no further infusions were given. Daily urinary urea nitrogen excretion during fasts when leucine was administered did not differ from values observed during control fasts. In protocol II, subjects were starved on two occasions for 14 d. During one fast, infusions of 11 mmol/d of alpha-ketoisocaproate were given on days 1--7; during the control fast, no infusions were given. Daily urine urea nitrogen excretion was lower (P less than 0.001) on days 1--7 and also on days 8--14 of the fast during which alpha-ketoisocaproate was given. The nitrogen-sparing effect of alpha-ketoisocaproate could not be related to changes in circulating levels of amino acids, ketone bodies, or insulin in either protocol. We conclude that alpha-ketoisocaproate infusions decrease the nitrogen wasting of starvation, whereas leucine, studied under identical conditions, does not.
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PMID:Nitrogen sparing induced by leucine compared with that induced by its keto analogue, alpha-ketoisocaproate, in fasting obese man. 746 28

Weight loss is a potent stimulus to food intake in normal individuals. The persistence of anorexia in wasting disorders, therefore, implies a failure of this adaptive feeding response. We describe a model for the normal hypothalamic response to starvation composed of the stimulation of neuronal pathways that promote energy intake and storage coupled with the inhibition of pathways that exert opposing effects. This model provides a framework for investigating disturbances of the normal hypothalamic response to weight loss and suggests a specific mechanism by which cytokines contribute to wasting in acquired immune deficiency syndrome and other cachexic disorders.
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PMID:Hypothalamic response to starvation: implications for the study of wasting disorders. 750 22

Anorexia, net proteolysis of skeletal muscle and consumption of body fat are hallmarks of the cachexia syndrome associated with chronic disease states. While inanition contributes to cachexia, this wasting diathesis has little in common with simple starvation. The cachexia syndrome is characterized by progressive weight loss and depletion of lean body mass in excess to that resulting from comparable caloric restriction. Accelerated mobilization and consumption of host protein stores from peripheral tissues occurs to support gluconeogenesis and acute phase protein synthesis [1, 2]. In contrast, simple starvation is associated with a relative sparing of lean tissue with the preferential consumption of fat. While the clinical manifestations of cachexia are readily apparent, identification of the specific mechanisms responsible for the development of cachexia remains an enigma. In recent years, interest has focused on the role that the immune system plays in the development of cachexia. Investigators initially hypothesized that the chronic production of two inflammatory cytokines, tumour necrosis factor alpha (TNF alpha) and/or interleukin-1 (IL-1), could explain the host non-specific responses resulting in cachexia [3-5]. Other pro-inflammatory cytokines, including interleukin-6 (IL-6) [6, 7] and interferon-gamma [8, 9], have been more recently proposed to be involved in this complex process. Although no consensus exists for the exclusive role of any one cytokine in the pathogenesis of cachexia, there is growing acceptance that the progression of cachexia results in part from the inappropriate release of one or more pro-inflammatory cytokines [10, 11]. In the present review, the current role of TNF alpha as a mediator of cachexia is examined.
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PMID:Tumor necrosis factor and cachexia: a current perspective. 788 18

Case report on 2,5 years old monozygotic twins who died of starvation due to negligence. Different gradings of protein-energy-malnutrition are discussed, among them the Waterlow-classification of PEM. The advantage of the Waterlow-classification is that stunting and wasting can be distinguished. The Waterlow-classification is suitable also for the classification of fatal cases of starvation in childhood. Practical experiences with own cases and cases from the literature are presented.
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PMID:[Starvation due to child neglect. Case report and aspects of expert testimony]. 797 67

Sepsis, shock, multiple trauma, and burns are often associated with altered metabolism characterized by severe catabolism, wasting of the lean body mass, immune dysfunction, and compromised wound healing. Nutrition support is one of the mainstays in the management of these critically ill patients and is aimed at minimizing these complications. The purpose of this article is to compare stress hypermetabolism and starvation metabolism, to review current recommendations for the provision of energy and substrate to the critically ill patient, and to review pertinent literature regarding enteral vs parenteral nutrition. Finally, this article will provide a brief overview of new and future therapies with emphasis on specific substrates and growth factors and the potential for their use in the critically ill patient.
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PMID:Nutrition support in critical illness. 807 50

Wasting may not be an inevitable consequence of HIV infection but may be a consequence of multiple nutritional insults that are additive without periods of replenishment in between. Protein energy malnutrition in AIDS patients may be consequential to underlying illness and concomitant to death as a result of that illness or may hasten a patient's demise, that is, starvation with fatal loss of body cell mass. Mortality is closely related to weight loss. Malnutrition may be a result of decreased intake, malabsorption, altered metabolism, or any combination of the three. Nutritional strategies to prevent PEM include appetite stimulation, early nutritional supplementation with oral supplements, and the diagnosis and treatment of malabsorption and underlying infections. More aggressive measures such as gastrostomy or jejunostomy tube placement and total parenteral feedings are still being evaluated. Nutritional supplementation to enhance the immune system or manipulate metabolism may be adjunctive to the above strategies. Early intervention and attention to nutritional status may have long-term benefits to patients with this disease.
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PMID:Nutritional aspects of HIV infection. 808 74

Nutritional support of patients with HIV or acquired immune deficiency syndrome (AIDS) has many similarities to other disease states in that the same nutritional products and techniques are used. Some patients with HIV, and many with AIDS without secondary infection, experience a metabolic milieu similar to patients with cancer cachexia. In providing dietary counselling to the HIV patient, we encounter many of the obstacles that must be overcome to improve nutrition in cancer: anorexia, gastrointestinal discomfort, lethargy, and poor nutrient utilization, which limit the ability for nutritional repletion. When a secondary infection is superimposed on HIV, patients resemble more highly catabolic trauma patients or patients in the intensive care unit (ICU), where, despite aggressive efforts to feed, there is usually a net nitrogen wasting leading to the more rapid development of cachexia. However, even in this setting, feeding will limit substantially net catabolism when compared to total starvation. Because the nutritional needs of HIV patients vary greatly, individual strategies have to be designed as the patient moves through the stages of disease. Patients are generally able to consume adequate nutrition either as regular food or dietary supplements during the latency period of viral replication. Once secondary infections become prevalent, artificial diets administered by tube or by vein may be required during the period of active secondary infections, with dietary supplements often helpful during more quiescent periods. Patients with HIV are among the most challenging for clinicians providing nutritional support. Knowledge from treatment of patients with other diseases may be useful, but more data must be gathered on the unique aspects of aetiology and treatment of the anorexia, malabsorption, and ultimate wasting associated with AIDS.
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PMID:Nutrition support and the human immunodeficiency virus (HIV). 811 86


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