PMID- 19318513
OWN - NLM
STAT- MEDLINE
DCOM- 20090716
LR  - 20211020
IS  - 0193-1849 (Print)
IS  - 1522-1555 (Electronic)
IS  - 0193-1849 (Linking)
VI  - 296
IP  - 6
DP  - 2009 Jun
TI  - Integration of hormonal and nutrient signals that regulate leptin synthesis and 
      secretion.
PG  - E1230-8
LID - 10.1152/ajpendo.90927.2008 [doi]
AB  - This review summarizes recent advances in our understanding of the pre- and 
      posttranscriptional mechanisms that regulate leptin production and secretion in 
      adipocytes. Basal leptin production is proportional to the status of energy 
      stores, i.e., fat cell size, and this is mainly regulated by alterations in 
      leptin mRNA levels. Leptin mRNA levels are regulated by hormones, including 
      glucocorticoids and catecholamines, but little is known about the transcriptional 
      mechanisms involved. Leptin synthesis and secretion is also acutely modulated in 
      response to hormones such as insulin and the availability of metabolic fuels. 
      Acute variations in leptin production over a time course of minutes to hours are 
      mediated at the levels of both translation and secretion. Increases in amino 
      acids and insulin after a meal activate the mammalian target of rapamycin (mTOR) 
      pathway, leading to an increase in specific rates of leptin biosynthesis. 
      Cross-talk among mTOR, PKA, and AMP-activated protein kinase pathways appears to 
      integrate hormonal and nutrient signals that regulate leptin mRNA translation, at 
      least in part through mechanisms involving its 5'- and 3'-untranslated regions. 
      In addition, the rate of leptin secretion from preformed stores in response to 
      hormonal cues is also regulated. Insulin stimulates, and adrenergic agonists 
      inhibit, leptin secretion, and this likely contributes to variations in the 
      magnitude of nutrition-related leptin excursions and oscillations. Overall, the 
      study of leptin production has contributed to a deepening understanding of leptin 
      biology and, more broadly, to our understanding of the cellular and molecular 
      mechanisms by which the adipocyte integrates hormonal and nutrient signals to 
      regulate adipokine production.
FAU - Lee, Mi-Jeong
AU  - Lee MJ
AD  - Division of Endocrinology, Diabetes, and Nutrition, Department of Medicine, 
      University of Maryland, School of Medicine, Baltimore, MD, USA.
FAU - Fried, Susan K
AU  - Fried SK
LA  - eng
GR  - DK52398/DK/NIDDK NIH HHS/United States
GR  - P30 DK072488/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20090324
PL  - United States
TA  - Am J Physiol Endocrinol Metab
JT  - American journal of physiology. Endocrinology and metabolism
JID - 100901226
RN  - 0 (Hormones)
RN  - 0 (Leptin)
SB  - IM
MH  - Adipose Tissue/*metabolism
MH  - Animals
MH  - Eating/physiology
MH  - Food
MH  - Hormones/*metabolism
MH  - Humans
MH  - Leptin/genetics/*metabolism
MH  - Obesity/*metabolism
MH  - Signal Transduction/*physiology
PMC - PMC2692400
EDAT- 2009/03/26 09:00
MHDA- 2009/07/17 09:00
PMCR- 2010/06/01
CRDT- 2009/03/26 09:00
PHST- 2009/03/26 09:00 [entrez]
PHST- 2009/03/26 09:00 [pubmed]
PHST- 2009/07/17 09:00 [medline]
PHST- 2010/06/01 00:00 [pmc-release]
AID - 90927.2008 [pii]
AID - E-90927-2008 [pii]
AID - 10.1152/ajpendo.90927.2008 [doi]
PST - ppublish
SO  - Am J Physiol Endocrinol Metab. 2009 Jun;296(6):E1230-8. doi: 
      10.1152/ajpendo.90927.2008. Epub 2009 Mar 24.