Circulating fetuin-A levels are not affected by short and long-term energy deprivation and/or by leptin administration.
OBJECTIVE
Fetuin-A may mediate cross-talk between the liver and adipose tissue. We studied the physiologic regulation of fetuin-A and explored its potential regulation by leptin.


METHODS
Fetuin-A levels were measured in three interventional studies as well as in in vitro experiments. Study 1: 15 lean subjects received placebo or physiologic replacement-dose recombinant human leptin (metreleptin) following short term complete caloric deprivation to induce severe hypoleptinemia; Study 2: 7 women with relative leptin deficiency due to strenuous exercise or low weight received 3 months of metreleptin; Study 3: 17 women with relative leptin deficiency were randomized to receive metreleptin or placebo over 9 months. In study 4 human hepatoma Hep G2 cells were treated with leptin. Fetuin-A mRNA expression and secretion were measured.


RESULTS
Complete caloric deprivation significantly decreased leptin but had no effect on fetuin-A levels. Normalizing leptin levels with metreleptin in hypoleptinemic subjects had no effect on circulating fetuin-A levels. Leptin treatment had no effect on fetuin-A mRNA expression and secretion in vitro.


CONCLUSIONS
Circulating fetuin-A levels are not affected by short and long-term energy deprivation. Furthermore, both in vivo and in vitro experiments confirm that fetuin-A is not regulated by leptin.
Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Beth Israel, Deaconess Medical Center, Harvard Medical School, Boston, MA.
Janice J
JJ
Hwang
Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Beth Israel, Deaconess Medical Center, Harvard Medical School, Boston, MA; Section of Endocrinology, Boston VA Healthcare System, Harvard Medical School, Boston, MA, 02130, USA; Section of Endocrinology, Diabetes, and Nutrition, Boston Medical Center, Boston University School of Medicine, Boston, MA. Electronic address: Bindiya.Thakkar@bmc.org.
Bindiya
B
Thakkar
Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Beth Israel, Deaconess Medical Center, Harvard Medical School, Boston, MA; Section of Endocrinology, Boston VA Healthcare System, Harvard Medical School, Boston, MA, 02130, USA.
John P
JP
Chamberland
Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Beth Israel, Deaconess Medical Center, Harvard Medical School, Boston, MA; Section of Endocrinology, Diabetes, and Nutrition, Boston Medical Center, Boston University School of Medicine, Boston, MA.
Christos S
CS
Mantzoros
D000273:Adipose Tissue / Q000378:metabolism; D000328:Adult; D000368:Aged; D031204:Caloric Restriction; D005260:Female; D006801:Humans; D020738:Leptin / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000097:blood*; D008099:Liver / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000378:metabolism; D013851:Thinness; D013997:Time Factors; D060749:alpha-2-HS-Glycoprotein / Q000235:genetics / Q000378:metabolism*
C556354:AHSG protein, human; D020738:Leptin; D012333:RNA, Messenger; D060749:alpha-2-HS-Glycoprotein; C415771:metreleptin
Alpha-2-Heremans-Schmid glycoprotein; Fetuin-A; Leptin