Immunohistochemical and ultrastructural localization of leptin and leptin receptor in human white adipose tissue and differentiating human adipose cells in primary culture.

Resistin Is a Key Mediator of Glucose-dependent Insulinotropic Polypeptide (GIP) Stimulation of Lipoprotein Lipase (LPL) Activity in Adipocytes

“…Following biosynthesis, leptin undergoes trafficking through the endoplasmic reticulum and Golgi network to reside in the limited cytoplasmic space surrounding the fat droplets (39,42). A fraction of adipocyte leptin appears to be localized in small vesicles (39,42,43). It is therefore possible that resistin also resides in intracellular vesicles and that GIP stimulates their production and secretion, as proposed for leptin (44).…”

“…The cellular mechanisms underlying secretion of the adipokines are still largely undefined. Following biosynthesis, leptin undergoes trafficking through the endoplasmic reticulum and Golgi network to reside in the limited cytoplasmic space surrounding the fat droplets (39,42). A fraction of adipocyte leptin appears to be localized in small vesicles (39,42,43).…”

Adipocyte Death and Chronic Inflammation in Obesity

“…Adipose tissue is now regarded as the largest endocrine organ that contributes to whole body metabolism through adipokine secretion. Other than adipocytes, immune cells such as macrophages have recently been discovered in adipose tissue (5). Subsequent studies demonstrated the significant role of adipose tissue macrophages in metabolic disorder associated with obesity (3).…”

Resting and circadian release of nitric oxide is controlled by leptin in male rats

“…Although leptin has been localized to the hypothalamic arcuate nucleus, in the very region where it controls NO release (3), the major storehouse of leptin is in the adipocytes (4). Therefore, it occurred to us that leptin released from the adipocytes might also activate NOS and cause release of NO.…”

“…Therefore, it occurred to us that leptin released from the adipocytes might also activate NOS and cause release of NO. † It has been shown that endothelial (e) NOS is present on the cell membrane of adipocytes (5), that leptin receptors are on their cell surface (4), and that they contain a significant storehouse of leptin in small pinocytotic vesicles beneath the cell membrane (4). We hypothesized that leptin is extruded by exocytosis from these vesicles and acts on its receptors on the surface of the adipocytes and on adjacent capillary endothelial cells to activate eNOS.…”