Hypotheses:

Fetal Malnutrition
HYPOTHESES:
The fetus receives an inadequate quantity of nutrients as a result of one or more mechanisms involving maternal malnutrition, placental malfunction or fetal genetic metabolic abnormalities. The fetal tissues respond to this deficient nutritional state by modifying their metabolic regulation to maximize the benefit from this nutritional deficiency. In 1992, Hales and Barker proposed the model of the thrifty phenotype suggesting that intrauterine malnutrition would lead to insulin resistance and decreased cell mass, thus predisposing to type 2 DM. According to this hypothesis, the endocrine alterations induced by intrauterine malnutrition are intended to divert the limited nutrient supply to maintain survival and development of vital organs, such as the brain, at the expense of growth. More recently, the fetal salvage hypothesis has been formulated. The finding that pre-pubertal IUGR children show a far greater insulin response than normal birth weight children, challenges the previously proposed cell hypoplasia. The fetal salvage model suggests that the malnourished fetus develops peripheral insulin resistance which allows a redistribution of nutrients -such as glucose- in favor of essential organs. This then leads to a permanent reduction in skeletal muscle glucose transporter number or function. This reduced peripheral insulin sensitivity stimulates cells to produce larger amounts of insulin to achieve normoglycaemia and would lead to eventual cell exhaustion. These metabolic changes become imprinted in the fetal brain and become permanently established. After birth, if excess or even adequate calories become available and the physical requirements are reduced, these calories are stored and visceral obesity occurs leading to insulin resistance and insulin resistance syndrome (IRS).

Fetal Malnutrition

Studies:

STUDIES:
The relationship between low birth weight and insulin resistance was studied in several population based studies. The first observations were that older adults with lowest birth weights had the highest rates of death form ischemic heart disease. Subsequently, cohorts of different populations were asked to participate in clinical evaluations. It was noted that the percentage of people aged 59-70 years who had impaired glucose tolerance (IGT) or type 2 DM fell progressively with increase birth weight, from 40% of those who weighed at birth 5.5 pounds or less to 14% of those weighed 9.5 pound or more. After these data were corrected to adult body mass index (BMI), individuals who were small babies were six times more likely to have IGT or type 2 DM independent of the gestational age of the baby indicating that the low birth weight rather than prematurity contributed to insulin resistance.

REFERENCES:
o Clinician's manual on insulin resistance. o http://fn.bmj.com/ o http://bmb.oxfordjournals.org/content/60/1/5.full

BY:
o DR. Mahmoud Ahmed Mahmoud Ahmed o Faculty of Medicine o Alexandria University

Fetal Malnutrition