Protein-energy malnutrition represents a shift of the body from fed to fasting/starvation state. Starvation leads to a decreased basal plasmainsulin concentration and in decrease of glucose-stimulated insulin secretion. Prolonged fasting results in a deficiency in amino acids used for gluconeogenesis. It is thought that kwashiorkor is produced by a deficiency in the adequate consumption of protein-rich foods during the weaning process. However, the associated edema is not fully understood. Several theories have been put forward to explain this finding. Marasmus on the other hand is thought to be due to the total caloric deficiency leading to wastingin a child. Marasmus always results from a negative energy balance.
Several studies have shown that a deficiency in the consumption of protein, carbohydrates and fat is responsible for the development of protein-energy malnutrition. However, other studies have proposed that chronic infections such as helminthicinfections are mainly responsible for the development of protein-energy malnutrition.[1] The underlying mechanisms include the following:
Hormonal and molecular mechanisms (fed to starvation state)[edit | edit source]
Protein-energy malnutrition represents a shift of the body from fed to fasting/starvation state.
The post-fed state may be considered as a useful reference point, as it denotes the period of metabolic transition from the fed to the fasted condition.
The major site of glucose utilization is the brain, which depends completely upon a continuous supply of glucose for oxidative metabolism during pot-absorptive state.
Maintenance of bloodglucose balance is achieved by the hepatic production of glucose at rates equal to those of tissue utilization.
In case of starvation, there is regulated and controlled production of ketone bodies causes a harmless physiological state known as dietary ketosis. In ketosis, the bloodpH remains within normal limits.[5]
The activity of mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase (mHS) is increased by starvation and a high-fat diet, and it is decreased by insulin.[10]
Eventual decreased gluconeogenesis in protein-energy malnutrition
Excessive oxidant stress was also proposed as a mechanism of development of kwashiorkor, however, it was discovered that that the administration of antioxidant was not successful in the prevention of the development of this malnutrition in a series of trials.
This has not been fully supported because evidence shows that neither the fecal microbiota transfer nor the local diet alone was sufficient to cause the malnutrition leading to the conclusion that changes in fecal microbiota are only effects rather than causes of kwashiorkor.[15][16][17]
Both in kwashiorkor and marasmus hair analysis is therefore advocated as a useful diagnostic procedure for both conditions. In both cases, there is a decrease in the amount of melanin present in the scalp hair.
↑Saudek CD, Boulter PR, Arky RA (1973). "The natriuretic effect of glucagon and its role in starvation". J. Clin. Endocrinol. Metab. 36 (4): 761–5. doi:10.1210/jcem-36-4-761. PMID4686383.
↑Scrimshaw NS, SanGiovanni JP (1997). "Synergism of nutrition, infection, and immunity: an overview". Am. J. Clin. Nutr. 66 (2): 464S–477S. PMID9250134.
↑Monk JM, Makinen K, Shrum B, Woodward B (2006). "Blood corticosterone concentration reaches critical illness levels early during acute malnutrition in the weanling mouse". Exp. Biol. Med. (Maywood). 231 (3): 264–8. PMID16514171.
↑Auphan N, Didonato JA, Helmberg A, Rosette C, Karin M (1997). "Immunoregulatory genes and immunosuppression by glucocorticoids". Arch. Toxicol. Suppl. 19: 87–95. PMID9079197.
↑Lefranc, Violaine; de Luca, Arnaud; Hankard, Régis (2016). "Protein-energy malnutrition is frequent and precocious in children with cri du chat syndrome". American Journal of Medical Genetics Part A. 170 (5): 1358–1362. doi:10.1002/ajmg.a.37597. ISSN1552-4825.