Abstract
Non-alcoholic fatty liver disease (NAFLD), which affects about a quarter of the global population, poses a substantial health and economic burden in all countries, yet there is no approved pharmacotherapy to treat this entity, nor well-established strategies for its diagnosis. Its prevalence has been rapidly driven by increased physical inactivity, in addition to excessive calorie intake compared to energy expenditure, affecting both adults and children. The increase in the number of cases, together with the higher morbimortality that this disease entails with respect to the general population, makes NAFLD a serious public health problem. Closely related to the development of this disease, there is a hormone derived from adipocytes, leptin, which is involved in energy homeostasis and lipid metabolism. Numerous studies have verified the relationship between persistent hyperleptinemia and the development of steatosis, fibrinogenesis and liver carcinogenesis. Therefore, further studies of the role of leptin in the NAFLD spectrum could represent an advance in the management of this set of diseases.
Highlights
Leptin is a 16 kDa adipocyte-derived hormone described for the first time by Zhang et al.(1994) as the product of the obese (Ob) gene [1], its existence was predicted some decades before in leptin-deficient and leptin receptor-deficient mice [2,3]
Insulin resistance (IR), adipose tissue inflammation and endothelial dysfunction may contribute to Non-alcoholic fatty liver disease (NAFLD) progression
IR was independently associated with serum leptin levels irrespective of adiposity and glycemic status in male prediabetic subjects
Summary
Leptin is a 16 kDa adipocyte-derived hormone described for the first time by Zhang et al. The most important leptin receptor is the long isoform Ob-Rb since it can fully transduce activation signals into the cell [9], including signaling pathways such as Janus kinase (JAK) 2/signal transducer and activator of transcription (STAT) 3, insulin receptor substrate (IRS)/phosphatidylinositol-3 kinase (PI3K), or Src homology 2 domain-containing phosphatase 2 (SHP2)/mitogen-activated protein kinase (MAPK) [10] This adipokine, leptin, is mostly recognized for playing a key role in the central control of both energy metabolism [11] and obesity [12], and has important regulatory functions in different physiological systems and diseases, such as reproduction [13], bone physiology [14], autoimmunity [15], and cancer [16], among many others [17].
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