According to the World
Health Organization, obesity is one of the leading causes of death in the
United States. Obesity increases the risk for other systemic diseases such as
diabetes, heart disease, high cholesterol, and more. In the busy lives that we
live here in the United States, it is just convenient and easy to resort to
fast food or frozen food for meals. Eating habits such as those are what are
causing people to gain weight and eventually become obese. However, studies have
been done to explore other possible factors that play a role in obesity such as
genetics and specific hormones.
This semester, Dr. Piedras came in to speak about her
research regarding leptin resistance in KHLH1 -/- hypothalamic neurons. Her study
was done with knockout mice. One of the experiments in the study involved
checking what the physiological concentrations of leptin does. Knockout neurons
are leptin-insensitive so therefore, any amount of leptin given to them will
not make a difference. It was found that partial blockage of t-type channels
restores leptin sensitivity to knockout neurons. The implications of this study
is that the t-type channels are means to control leptin and can be used to
screen for treatments for obesity.
Recently, there was a study in the Cell Metabolism Journal on diet-induced obese mice to explore
endogenous leptin activity in obesity. Obesity is a state of hyperleptinemia
and low levels of response to exogenous leptin. Leptin is a hormone released
from adipose tissue in order to signal satiation. Studies show that those who
lack leptin are often overweight. Diet-induced
obesity is a more common form of obesity which shows hyperleptinemia. It is
also important to note that leptin impairment is associated with leptin resistance—resistance
implies the inability of leptin to reduce feelings of hunger. The purpose of this study is to use genetic
and diet-induced models of mice in order to see if the inhibition of the leptin
receptor resulted in any changes in food intake and body weight.
In this study, both lean and obese mice were treated with
leptin receptor antagonist. It was found that, with treatment of antagonist
leptin, the lean mice increased feeding and body weight. These results were not
seen in the obese mice. Additionally, there was an increase feeding and body
weight due to the antagonist seen in lean and diet-induced obese mice. Based on
these findings, the researchers concluded that hyperleptinemic diet-induced
mice undergo leptin suppression as opposed to lean mice. The findings also
suggest that endogenous leptin resistance is a factor to the obesity in
diet-induced obese mice. The implications of this study are important when
screening for obesity. If the factors that are involved in obesity are better
understood, then proper action can be taken to avoid such weight gain or to
better treat it.
With the increasing rate of obesity in the country, it is
important that enough research is conducted on the causes and factors that play
a role in obesity. This will help to better understand how to treat and prevent
such diseases.
References:
http://www.who.int/mediacentre/factsheets/fs311/en/
Science Direct. “Diet-Induced Mice Retain Endogenous Leptin
Action.” Cell Metabolism Journal 21.6
(2015): Pages 877-82. http://www.sciencedirect.com.flagship.luc.edu/science/article/pii/S1550413115001709?np=y
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