Differential expression of factors involved in fat metabolism with age and the menopause transition.
OBJECTIVE
Changes in the hormonal milieu at the menopause are associated with an increase in total adiposity and a more android pattern of fat distribution, with the latter associated with an increased risk of the metabolic syndrome. The aim of this study was to explore potential mechanisms that might contribute to the changes in body composition associated with the menopause transition.


METHODS
Using real-time PCR analysis, we have compared the expression of various factors involved in fat metabolism in subcutaneous abdominal and gluteal fat in premenopausal (Group 1; n=11), postmenopausal (Group 2; n=10) and postmenopausal women taking estrogen therapy (Group 3; n=10).


RESULTS
All subjects were of normal body mass index, euglycemic and normolipemic. The postmenopausal women were older (Group 1, 43.1+5.0 versus Groups 2 and 3, 57.9+/-7.4 years, P<0.001 and 56.1+/-4.5 years, P<0.001, respectively). Expression analysis revealed that levels of transcripts encoding adiponectin, peroxisome proliferator-activated receptor gamma and fatty acid transporter, each associated with insulin sensitivity, were significantly greater in gluteal fat from estrogen deplete postmenopausal women than in fat from the other two groups (P<0.05). In contrast, levels of transcripts for acetyl CoA carboxylase alpha, long chain acyl CoA dehydrogenase and hormone sensitive lipase were significantly greater in abdominal fat from premenopausal women than either postmenopausal groups (P<0.05).


CONCLUSIONS
These findings indicate both aging and the menopause transition are associated with changes in fat metabolism, which may contribute to the accumulation of body fat after menopause.
Prince Henry's Institute of Medical Research, Clayton, Vic. 3168, Australia.
Marie L
ML
Misso
Christina
C
Jang
Jennifer
J
Adams
Jane
J
Tran
Yoko
Y
Murata
Robin
R
Bell
Wah Chin
WC
Boon
Evan R
ER
Simpson
Susan R
SR
Davis
D000103:Acetyl-CoA Carboxylase / Q000235:genetics; D044942:Acyl-CoA Dehydrogenase, Long-Chain / Q000235:genetics; D052242:Adiponectin / Q000235:genetics; D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism*; D000328:Adult; D000368:Aged; D000375:Aging / Q000235:genetics / Q000378:metabolism*; D001823:Body Composition / Q000235:genetics / Q000502:physiology*; D015992:Body Mass Index; D015914:Estrogen Replacement Therapy; D050612:Fatty Acid Transport Proteins / Q000235:genetics; D005260:Female; D015870:Gene Expression; D006801:Humans; D020738:Leptin / Q000235:genetics; D008593:Menopause / Q000235:genetics / Q000378:metabolism*; D008875:Middle Aged; D047495:PPAR gamma / Q000235:genetics; D016133:Polymerase Chain Reaction; D011972:Receptor, Insulin / Q000235:genetics; D002787:Sterol Esterase / Q000235:genetics
D052242:Adiponectin; D050612:Fatty Acid Transport Proteins; D020738:Leptin; D047495:PPAR gamma; D044942:Acyl-CoA Dehydrogenase, Long-Chain; D011972:Receptor, Insulin; D002787:Sterol Esterase; D000103:Acetyl-CoA Carboxylase