Leptin Secretion by Adipose Tissue and Gastric Mucosa for the Control of Food Intake: A Review

Special Article - Oral Administration of Leptin

Austin J Endocrinol Diabetes. 2016; 3(3): 1048.

Leptin Secretion by Adipose Tissue and Gastric Mucosa for the Control of Food Intake: A Review

Bendayan M* and Cammisotto PG

Department of Pathology and Cell biology, University of Montreal, Canada

*Corresponding author: Bendayan M, Department of Pathology and Cell biology, University of Montreal, C.P. 6128 Succ. Centre Ville 2900 Edouard MontPetit Montreal, Quebec, H3C 3J7, Canada

Received: July 05, 2016; Accepted: August 23, 2016; Published: August 26, 2016


Endocrine and exocrine secretion of leptin by adipose tissue and gastric mucosa respectively is reviewed. Both the adipocytes and the gastric chief cells synthesise leptin and process it through the RER-Golgi-granule secretory pathways. However, while adipocytes process leptin through a slow constitutive endocrine secretion, the gastric cells release leptin through a rapid regulated exocrine secretion into the gastric juice. Both types of cells secrete a peptide bound to the soluble isoform of its receptor. The leptin-leptin receptor complex released by the chief gastric cells is able to resist the harsh hydrolytic conditions of the gastric cavity. It is then vehiculated by the gastric juice to the duodenal lumen in an intact active form. Leptin then interacts with its own transmembrane receptor present on the luminal plasma membrane of the intestinal cells. Upon internalization in the endocytotic compartment, leptin is channelled towards the Golgi apparatus of the intestinal cell where it binds again to its soluble receptor. The leptin-leptin receptor complex is then released by the epithelial cells towards the connective tissue and reaches the blood circulation. It reaches the central nervous system for the control of food intake. Molecular and cellular mechanisms involved in secretion of leptin by the gastric chief cells, its transfer to the duodenal lumen, its internalization by the intestinal enterocytes and its release towards circulation are reviewed and summarized.

Keywords: Leptin; Gastric mucosa; Intestinal mucosa; Adipose tissue


Many factors such as abundance of food, easy availability, media advertising, large variety of processed ready-made meals, lack of physical exercise and sedentary social life style associated with psychological issues, is contributing since at least 50 years, to an epidemic problem of obesity in our society [1]. Understanding the regulation of food intake has become increasingly complex not only because of the many hormones both orexigenic and anorexigenic that play key roles in the control of appetite, but also because intervention of emotional more complex aspects. One area in the brain appears to be the main conductor in this field. The hypothalamic gland is the center of control for food intake responding to signals emerging from various origins for the maintenance of a delicate balance between hunger and satiety.

One of the key players in this ensemble appears to be leptin, a hormone that regulates our appetite and restrain the amount of food ingested. Predicted in the 1950s by Kennedy [2] and Hevrey [3] in their lipostatic theory, this hormone and its gene were only identified much later in the 1990s by Friedman [4]. The hormone was named after the Greek word «leptos» meaning «thin» [4-8]. Indeed, lack of the leptin gene, as it occurs in a particular strain of mice, the ob/ob mice, leads to an inability to have satiety sensations with hyperphagy and obesity.

Leptin from adipocytes

The primary source of leptin and the first organ having been identified as secreting this hormone is the white adipose tissue [9,10].

Leptin immunolabeling of adipose tissue revealed the presence of the hormone within the small cytoplasmic ring that surrounds the large lipid droplet of the adipocytes [11] (Figure 1). The hormone was localized by immunoelectron microscopy along the RER-Golgigranules secretory pathway [11] (Figure 2). In fact, leptin has been the first hormone detected in adipose tissue which is now recognized as an endocrine gland [12]. Leptin is being secreted by the adipose tissue in a slow constitutive fashion which means that it is synthesized and secreted continuously [13]. Leptin cellular content and amounts released remain constant at all times. Adipocytes maintained in cell culture which secrete steady amounts of leptin require an hour of stimulation of secretion to increase their leptin synthesis and release (Figure 3) [11,13].