Stimulation of leptin release by arachidonic acid and prostaglandin E2 in adipose tissue from obese humans

Fain, John N.; Leffler, Charles W.; Cowan, George S M; Buffington, Cynthia; Pouncey, L; Bahouth, Suleiman W.

doi:10.1053/meta.2001.24927

Cited by 49 publications

(36 citation statements)

References 30 publications

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“…We found direct association of arachidonic acid with leptin in women. No previous epidemiological study examined this relationship, Fain et al found that arachidonic acid stimulated leptin release by explants of subcutaneous adipose tissue from obese humans [26]. This relation in our study also was not independent of BMI.…”

Section: Discussioncontrasting

confidence: 48%

Relation of dietary and lifestyle traits to difference in serum leptin of Japanese in Japan and Hawaii: The INTERLIPID study

Nakamura

Ueshima

Okuda

et al. 2012

Nutrition, Metabolism and Cardiovascular Diseases

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Section: Discussioncontrasting

confidence: 48%

Relation of dietary and lifestyle traits to difference in serum leptin of Japanese in Japan and Hawaii: The INTERLIPID study

Nakamura

Ueshima

Okuda

et al. 2012

Nutrition, Metabolism and Cardiovascular Diseases

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“…33,38 Studies also have shown that prostaglandin E2 stimulates leptin secretion from cultured human adipose-tissue cells and that COX2 inhibitors prevented the increased leptin production. 39 Our results showed a statistically significant interaction between recent use of aspirin/NSAIDs and LEP polymorphisms suggest that leptin may influence colon cancer through mechanisms involving COX2 inhibitors and that greater pro-inflammatory response possibly associated with genotype may be modified by aspirin/NSAID.…”

Section: Discussionmentioning

confidence: 57%

Leptin and leptin receptor genotypes and colon cancer: Gene–gene and gene–lifestyle interactions

Slattery

Wolff

Herrick

et al. 2008

Intl Journal of Cancer

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Leptin may play an important role in colorectal cancer because of its role in energy balance, insulin and inflammation. We evaluated the LEP rs2167270 (19 G > A) and rs7799039 (22548 G > A) poly-morphisms and the leptin receptor, LEPR rs6588147 (located in intron 2), polymorphism with risk of developing colon cancer in a study of 1,567 cases and 1,965 controls. We evaluated the effects of the polymorphisms with body mass index (BMI), recent use of aspirin/NSAIDs and genetic variations in genes related to insulin signaling pathways including insulin-like growth factor 1 (IGF1), insulin-like growth factor binding protein 3 (IGFBP3), and insulin related substrates 1 and 2 (IRS1, IRS2) and the vitamin D receptor (VDR). We observed a slight reduction in colon cancer risk with the AA LEP rs2167270 genotype (OR 0.79 95% CI 0.64, 0.98) and although not reaching statistical significance, with the combined GG LEP rs2167270 and GG LEPR rs6588147 (OR 0.70, 95% CI 0.49, 1.02) genotypes. BMI did not interact with any of these polymorphisms to alter colon cancer risk. However, recent aspirin/NSAID use significantly interacted with both LEP poly-morphisms. Likewise, variants of IGF1 and IRS2 interacted with the LEP rs2167270 polymorphism. VDR polymorphisms interacted with all LEP and LEPR polymorphisms. These data support an association between LEP and colon cancer. They also suggest that the mechanisms linking leptin to colon cancer may be independent of energy balance. ' 2007 Wiley-Liss, Inc. Leptin is a 16 kDa glycolprotein product of the leptin gene (LEP), which is expressed almost exclusively (>95%) by adipo-cytes. 1 Initial interest in leptin focused on its role in obesity but it is rapidly becoming evident that its physiological properties extend beyond those associated with energy homeostasis. In addition to regulation of energy balance, leptin, has been associated with reproductive factors, inflammatory response, insulin signal-ing, bone remodeling and neuroendocrine function. 2 The leptin receptor , a class I pro-inflammatory cytokine, is a member of the cytokine receptor family that includes IL-6. The leptin receptor plays a key role in how leptin functions. When leptin binds to the leptin receptor, Janus kinase (JAK2), a tyrosine kinase is activated to initiate downstream signaling of suppressors of cytokine signal-ing 1 and 3 (SOCS) and signal transducer and activator of transcription -3 (STAT). 2-4 Of particular importance for cancer is the influence of leptin on SOCS which in turn limits insulin signaling; SOCS3 has been shown to limit leptin signaling. Studies have shown that leptin also can stimulate expression of the inflamma-tory marker CRP (C-reactive protein). 5 There is growing evidence that nuclear hormone receptors regulate the action of leptin and other class I cytokines. 6 However, data also suggest that hormone receptors, such as the vitamin D receptor , might play an important role in regulating leptin; vitamin D 3 has been shown to inhibit leptin secretion in human adipose tissue. 7 Leptin has been ...

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“…In contrast, Fain et al [114] showed that PGE2 stimulated leptin release from cultured mouse adipose tissue. In another study, leptin secretion by explants of human adipose tissue obtained from obese individuals was enhanced by both PGE2 and its metabolic precursor, arachidonic acid [115]. Increased leptin production in the presence of arachidonic acid is reduced by selective pharmacologic inhibition of the cyclooxygenase 2 (COX-2) isoenzyme.…”

Section: Leptin and Cancermentioning

confidence: 99%

Leptin is a growth factor in cancer

Somasundar

McFadden

Hileman

et al. 2004

Journal of Surgical Research

153

119

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Stimulation of leptin release by arachidonic acid and prostaglandin E2 in adipose tissue from obese humans

Cited by 49 publications

References 30 publications

Relation of dietary and lifestyle traits to difference in serum leptin of Japanese in Japan and Hawaii: The INTERLIPID study

Relation of dietary and lifestyle traits to difference in serum leptin of Japanese in Japan and Hawaii: The INTERLIPID study

Leptin and leptin receptor genotypes and colon cancer: Gene–gene and gene–lifestyle interactions

Leptin is a growth factor in cancer

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