The high prevalence of anthropometric measurements and laboratory values that are similar to those in patients with protein-energy malnutrition has lead to the classification of a large number of dialysis patients as being malnourished. However, malnutrition in the strict sense implies that abnormalities will be reversed if more food is eaten. There is virtually no evidence, however, that simply providing more nutrients in the diet of dialysis patients will reverse the abnormalities attributed to malnutrition. This suggests that the diagnosis of malnutrition is a misdiagnosis. In this review, we discuss mechanisms that will cause the loss of protein stores, including albumin, other plasma proteins, and muscle mass in dialysis patients. We will also review the shortcomings of techniques that are used to measure the nutritional status of these patients.
The effects of during early life on acetylcholinesterase (AChE) specific activity of , and were examined in rehabilitated adults . Undernourished rats were raised by dams maintained on a scheme from pup birth to pup weaning. The offspring were maintained on a restricted food schedule until day 38 when they started to have free access to food until 70-80 days of age. Control rats were raised by dams which had free access tofood. The results showed that early malnutrition caused a significant increase in AChE specific activity in cerebellum (about 20%), striatum (about 40%), and hypothalamus (about 30%). No changes were found in the hippocampus. Undernutrition caused a significant increase in Vmax when compared to the control group without changes in Km both in cerebellum and striatum. These results suggest that early undernutrition changes AChE concentration in cerebellum and striatum and does not affect the affinity of the enzyme for the substrate.
The efect of stressful stimulation and protein malnutration on the gonadotrophic and somatotrophic axis of sheep is discussed with special references to the relatioship between these stimuli and the GnRH and somatostatin neuronal system in the hypothalmus.Generally, long-term stimulation and chronic underfeeding reduce gonadal functions in the sheep.There is evidence for the GnRH-dependent pathway for the mechanism of these phenomena in femle sheep.GnRh neurons respond to long-term stress in diminishing of neuropeptide release from the nerve terminals due to the depression of its axonal transport.Chronic restriction of dietary proteins in lambs reduces the plasma LH concentration but does not impair the development of GnRH neurons nor the synthesis and processing of GnRH.It is suggested that malnutrition delays the first ovulation probably due to the neural mechanism responsible for the preovulatory GnRH/LH output.Stress has rather unclear effect on growth hormone (GH) secretion in the sheep.Prolonged, but not short stressful stimulation provokes the rapid release of somatostatin, which is sustained during long-term stimulation.These results suggest that effect of stress on somatotrophic axis depends on the period of stressful stimulation.VChronic malnutrition enhances secretion of GH by an increse in amplitude of GH pulses and reduces the secretory activity of somatostatin neurons.It is postulated that nutrients can influence GH secretion in the sheep by mechanism dependent on the hypothalmic somatostatin.
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