A Review of the Leptin Hormone and the Association with Obesity and Diabetes Mellitus

Aldeam Facey, Lowell Dilworth and Rachael Irving
Published Date: March 08, 2017

Abstract

Leptin is a protein hormone that regulates food intake. It is secreted by the adipocytes and contains 167 amino acids. The hormone signals the hypothalamus and is released to reduce the desire for food thereby controlling appetite. Research shows that diet-induced obesity results in leptin resistance, so while the level of leptin may be high, it is ineffective.

Leptin is also increased in type 2 diabetes mellitus which is strongly associated with obesity and insulin resistance. While leptin may be elevated in both diabetes and obesity, it is not the cause of either disease. It has been suggested that leptin mediates insulin resistance and as such may be a possible treatment for insulin resistance.

Diet induced leptin resistance can be reversed through dietary changes and its administration can be effective in combating insulin resistance. Leptin levels may also decrease with increased exercise.

The pathophysiology involving leptin resistance is unclear. More leptin studies are needed as it may be an unexplored treatment for diabetes and may be able to provide a more detailed understanding of the disease.

Leptin and diabetes

Type 2 diabetes is expected to afflict 300 million persons by 2020 [22]. Not many studies have assessed a direct relationship between leptin concentration and diabetes [23]. Research has however shown that leptin levels are generally higher in persons with diabetes mellitus except when the data is adjusted for body mass index [23].

Leptin has the ability to improve or conversely induce insulin resistance [24]. This hormone is also known to mediate the release of insulin from pancreatic β cells [24]. Research shows that leptin can be therapeutically useful in the treatment of lipoatrophic diabetes [25]. It is interesting to note that obesity is directly associated with insulin resistance and the development of diabetes mellitus in humans [24].

Given that obesity can be a result of leptin resistance, leptin resistance is likely to be involved in the development of the disease. Like Leptin resistance, leptin deficiency is significant in the pathogenesis of severe insulin resistance in uncontrolled insulin deficient diabetes mellitus [26].

It can however be noted that leptin signaling in neurons can be restored by overexpression of anorexigenic peptides and or repression of orexigenic peptides [27]. Food compounds such as teasaponins, reservatrol, caffeine, taurine and celastrol are able to restore the leptin signaling in neurons using the expression or repression of these peptides [27].

It was also discovered that vitamins A and D improves the transport of leptin across the blood brain barrier [27]. Researchers found that leptin treatment reverses diabetes in lipoatrophic mice [28]. Diet and leptin treatment should be thoroughly explored as a method of diabetes control.

Conclusion

Leptin elevation in diabetes and obesity makes it a significant parameter to assess in clinical research studies. For years it has been known that obesity associated diabetes is linked to insulin resistance as the central basis for the association [37]. Leptin is involved in energy metabolism and changes with physical exercise.

Leptin has also been found to have immunological responses [38]. Its signaling can regulate innate inflammatory responses, regulate adaptive immunity and even suppress regulatory T cell differentiation [38]. To date the link between insulin resistance and obesity is not clearly defined as details of the mechanism are not fully understood [37].

Further studies on leptin metabolism and mechanisms of action may be able to define or fill the gap that exists. Research can also explore leptin therapy in combination with dieting which stimulates leptin signaling as a means of controlling diabetes and obesity.