a genetic disorder characterized by excessive appetite, massive obesity, short stature, and intellectual disability
Prader-Willi syndrome
although an individual’s genetic inheritance may make obesity likley
push by environmental factors that encourage energy consumption and discourage energy expenditure
promotes fat storage in fat cells and muscle cells
lipoprotein lipase (LPL)
high LPL activity makes normal energy intake cause
more dramatic impact in fat storage
obesity gene codes for leptin
ob gene
a hormone primarily produced and secreted by the fat cells in proportion to the amount of fat stored
leptin
leptin surpresses the appetite, increases energy expenditure, and produces fat loss
in hypothalamus
suppression of leptin production, increased appetite, and decreased energy expenditure
fat loss produces
mice with defective obesity gene
don’t produce leptin and weight three times normal size
leptin resistance
the normal production of leptin but failure to respond to it
is synthesized and secreted primarily by the stomach cells but works in the hypothalamus to promote a positive energy storage
ghrelin
triggers desire to eat
ghrelin
high ghrelin levels
low body weight
the number of fat cells increases most rapidly during
growing years of late childhood and early puberty
after growth ceases
fall cells expand in size