Got Food? - the Scientia Review

one study, research examined two children of Pakistani origin who were severely obese. Both had
extremely low levels of leptin in their bloodstreams. In fact, both children had a homozygous mutation of
the leptin and melanocortin receptor gene, which, scientists now know, is associated with cases of morbid
obesity (Farooqi, 2005). In a later study, however, researchers ascertained that heterozygous combinations
of the leptin gene and its receptors have shown had minimal impact on body weight control. In order to
fight childhood obesity resulting from leptin deficiencies, scientists have attempted leptin therapy, in
which the hormone is regularly injected into the bloodstream. Three children were administered leptin
doses for 48 months, and all three showed significant reductions of body weight, of which 98% was body
fat.
Other hormonal abnormalities arising from genetic mutations associated with adolescent obesity
include deficiencies in the melanocortin 4 receptor and prohormone convertase 1. Since the late 20th
century, mutations, in the melanocortin 4 receptor have been linked to adolescent obesity. Experts suspect
that receptor trait is dominant because some studies have shown that 100% of the subjects who posessed
heterozygous mutations also demonstrated obese phenotypes. However, further investigation is necessary
because other analysis has shown that homozygous carriers of the trait were reported to be more obese
than carriers with heterozygous combinations. MC4R deficiencies causes hyperphagia and an increased
amount of fat mass. In addition, scientists have noted an accumulation of lean mass and noteworthy
heightened levels of bone mineral density (Farooqi, 2005).
Hormonal levels play a significant
role in childhood obesity.
Other Hormonal Causes of Obesity
In addition to leptin, and melanocortin, other hormones have been examined for their role in the
development of childhood obesity. One such hormone is adiponectin, a protein hormone which controls
many metabolic processes including, glucose regulation and fatty acid catabolism. Adiponectin is released
from the adipose tissue, and its levels in the bloodstream are inversely proportional to the body fat
percentage. The hormone promotes energy expenditure, and as a result has been analyzed in studies
pertaining to obese children. In one report, researchers observed the levels of adiponectin in obese and
non-obese children of Greek descent. The adiponectin levels in the obese subjects were significantly
lower than the levels of the non-obese subjects. In addition, the adiponectin levels steadily decreased as
the subjects went through puberty, which further exascerbated the obesity issue. Further, male adolescents
had the lowest levels of adiponectin, and later studies revealed a relationship between the adiponectin
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