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Gibson, W. T., Farooqi, I. S., Moreau, M., DePaoli, A. M., Lawrence, E., O'Rahilly, S., & Trussell, R. A. (2004). Congenital Leptin Deficiency Due to Homozygosity for the Delta133G Mutation: Report of Another Case and Evaluation of Response to Four Years of Leptin Therapy. The Journal of Clinical Endocrinology & Metabolism, 89, 4821-4826.
https://doi.org/10.1210/jc.2004-0376

has been cited by the following article:

• TITLE: Critically Discuss the Revival of Leptin for Obesity Therapy

  AUTHORS: Chi-Fai Lo

  KEYWORDS: Obesity, Energy Homeostasis, Leptin Difficency, Leptin Resistance, Leptin Sensitisers, Leptin Receptors

  JOURNAL NAME: Psychology, Vol.9 No.2, February 12, 2018

  ABSTRACT: Obesity has created a very serious public health problem, and World Health Organisation has actually warned that there is an urgent need for multinational cooperation to stem the rise of obesity. More than 20 years ago the discovery of Leptin, which is an adipocyte-secreted hormone and primarily acts on the hypothalamic neurons to activate the regulation of energy homeostasis, created much interest in its potential use for the treatment of obesity, but the hope was soon lost after leptin failed to counteract common diet-induced obesity. In recent years some preclinical studies have surprisingly demonstrated that resistance to leptin can be reversed and the effects of leptin therapy can be amplified by several leptin sensitisers. This paper will critically discuss the plausible revival of leptin for obesity therapy with reference to research findings on various influencing factors contributing to the level of expression and secretion of leptin.