Research Paper on A Historical Perspective of Leptin

Introduction

The research is based on obesity and diabetes. The researcher participated in the analysis to understand the physiologic basis of the chronic diseases. The investigation tries to find the genetic difference between normal mice and those affected by diabetes or obesity. The result is the discovery of a hormone that regulates satiety named Leptin. The discovery of this hormone assists in explaining the outcome experienced from the numerous experiments done and validates most of the predictions made in the course of the research (Coleman, 2010).

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The mouse is used as the basis of understanding the diseases and the genetics associated with them. The researcher utilizes three genetically different mice. The first mouse used is the ob/ob mouse discovered in 1950 and used as a model for mild diabetes. The mouse has an ob mutation on chromosome 6, and this clinically presents as massive obesity, hyperphagia, and transient diabetes. The second mouse is an obese mutant named db/db mouse discovered in 1965. The db mutation is located in chromosome 4, unlike the ob mouse. The db mouse is similar to the ob mouse in that it also develops massive obesity and hyperphagia but differs in that it also develops severe life-shortening diabetes.

The researcher's interest is in discovering the possible presence of a circulating factor that is responsible for this obese phenomenon - the interest in the discovery of an element in normal mice that could prevent obesity or mitigate the metabolic abnormalities. The other option is the discovery of the factor in the mutant mice that could cause obesity in the normal mice. The first step is to establish a circulatory connection between the mice and observe the effects or presentation of the syndromes and from the result draw possible hypotheses. Parabiosis is described as a procedure in which two mice of the same genetic background are surgically joined through anastomosis of their skin from the shoulder to the pelvic girdle.

The first experiment involved a db/db mouse paired with a normal mouse through Parabiosis and after wound healing around the anastomosis the pair was observed. The result was the death of the standard mouse even after numerous repetitions to rule out poor surgery as a result of the death. Necropsy done on the regular mouse showed that the standard mouse lacked food in their stomach and did not have food remnants in the intestines. The liver of the normal mouse had no detectable glycogen once the tests were done. The diabetic mouse maintained elevated blood sugars and had food present in its stomach. The assumption from this first experiment was that the diabetic mouse produced blood-borne satiety factor of increased strength that in limited amounts from cross-circulation induced starvation in the normal mouse.

The ob/ob mouse paired through parabiosis with the db/db mouse resulted in a decline of the blood sugar in the ob mouse to starvation levels with a survival time ranging 20-30 days. The necropsy results showed a reduction in the adipose tissue mass of the ob mouse and stomach free of food. The db mouse, however, maintained an elevated blood sugar and gained weight. Parabiosis of the ob mouse and the normal mouse resulted in positive effects for the ob mouse. The mutant mouse's weight gain was slowed down, and the food consumption of the pair was reduced to the amount consumed by normal mice. The overall conclusion is that the db mouse produced the satiety factor in excess and was resistant to the hormone while the ob mouse was sensitive to the element but produced inadequate amounts of the satiety factor.

Eventually, the satiety factor was identified as Leptin by Jeffrey Friedman. It is a hormone produced by the adipose tissue and has receptors at the hypothalamus. This discovery has developed the management of obesity and other conditions resulting from the deficiency of the factor. Combination therapy involving leptin will revolutionize the management of obesity.

References

Coleman, D. (2010). A Historical Perspective on Leptin. Nature America.