Elucidation of the mechanism of action of leptin would help to develop novel therapeutic approaches for there metabolic disorders like obesity and diabetes.
Obesity induces abundant leptin production, however, reduced sensitivity to leptin leads to the development of metabolic disorders, so called leptin resistance.
Our results suggest that metabolic disorders in normal weight children are associated with a high monosaccharide intake and elevated bacterial endotoxin as well as leptin plasma levels, the latter also discussed as being indicative of visceral adiposity.
In this review, the studies on leptin neural and cellular pathways are summarized with an emphasis on the progress made during the last 10 years, for better understanding the molecular mechanism of obesity and other metabolic diseases.
In summary, the evidence suggests that leptin is both a target and a mediator of epigenetic changes that develop in numerous tissues during metabolic disorders.
Here, we summarized the advances and controversy of leptin resistance and associated diseases, for better understanding the physiology and pathophysiology of leptin as well as the new strategies for treating obesity and metabolic disorders.
The adipokines DPP-4 and leptin in the serum can influence the body fat distribution of patients with T2MD; there is an important association of DPP-4, leptin and ADPN levels with MS, which may be used as therapeutic targets for multiple metabolism disorders of T2MD.
The results provide new information about associations between leptin, sex-specific weight and appetite changes and problematic eating behaviours, which may be risk factors for cardiovascular and metabolic diseases in MDD, particularly in females.
Mouse models of obesity (ob/ob) and diabetes (db/db) in which the leptin (Lep) and leptin receptor (Lepr) genes have been mutated, respectively, have contributed to a better understanding of human obesity and type 2 diabetes and to the prevention, diagnosis, and treatment of these metabolic diseases.
This review discusses the latest data regarding the role of leptin as a mediator of immune system and metabolism, with particular emphasis on its effects on obesity-associated metabolic disorders and autoimmune and/or inflammatory rheumatic diseases.
To determine whether leptin resistance is a cause or a result of DF-induced obesity with metabolic disorders, we restricted the feeding times of leptin resistant db/db mice.
Increasing adiposity contributes to a worsening imbalance of pro- and anti-inflammatory adipokines over time, in which leptin may have an important role as a key mediator of metabolic disease risk in Mexican Americans.
The use of microorganisms with low and medium inflammatory properties and ability to modulate leptin levels could be a strategy for the treatment of some metabolic diseases associated with dysregulation of immune response.
Leptin is an approved treatment for generalized lipodystrophy, a condition associated with severe metabolic disease, and has also shown potential for the treatment of other types of diabetes.
In addition, besides specific T helper subsets and their cytokine products, the roles of the scavenger receptors, the inflammasome, the newer cytokines of the IL-1 (e.g., IL-33, IL-37) and IL-12 (e.g., IL-27, IL-35) families, and the soluble mediators produced by adipocytes (adipokines) (e.g., leptin, adiponectin) in the pathogenesis of inflammation, autoimmunity, and metabolic disorders are increasingly being realized.
The discovery of leptin not only revolutionised our understanding of endocrine physiology but has also resulted in a registered medicinal product which is already improving the health of patients with serious metabolic diseases.
This study indicates that leptin may act as a growth-promoting signal during fetal development, and suggests a possible role for the LEPR in explaining the inverse relationship between birth weight and the development of metabolic diseases in adulthood.
In conclusion, adipose tissue AKR1C3 expression may be affected by metabolic disease, and its levels are significantly reduced in response to dietinduced weight loss and correlate with leptin levels.