Postprandial triglycerides and adipose tissue storage of dietary fatty acids: impact of menopause and estradiol

Abstract

Objectives: Postprandial lipemia worsens after menopause, but the mechanism remains unknown. The hypothesized menopause-related postprandial lipemia would be (1) associated with reduced storage of dietary fatty acids (FA) as triglyceride (TG) in subcutaneous adipose tissue (SAT) and (2) improved by short-term estradiol (E2 ).

Methods: Twenty-three pre- (mean ± SD: 42 ± 4 years) and 22 postmenopausal (55 ± 4 years) women with similar total adiposity were studied. A subset of postmenopausal women (n = 12) were studied following 2 weeks of E2 (0.15 mg) and matching placebo in a random, cross-over design. A liquid meal containing (14) C-oleic acid traced appearance of dietary FA in: serum (postprandial TG), breath (oxidation), and abdominal and femoral SAT (TG storage).

Results: Compared to premenopausal women, healthy, lean, postmenopausal women had increased postprandial glucose and insulin and trend for higher TG but had similar dietary FA oxidation and storage. Adipocytes were larger in post- compared to premenopausal women, particularly in femoral SAT. Short-term E2 reduced postprandial TG and insulin but had no effect on oxidation or storage of dietary FA. E2 increased the proportion of small adipocytes in femoral (but not abdominal) SAT.

Conclusions: Short-term E2 attenuated menopause-related increases in postprandial TG and increased femoral adipocyte hyperplasia but not through increased net storage of dietary FA.

Figure 1

Schematic timeline for 24-hour test meal visit. Fasting and postprandial blood samples (¹⁴C-TG), breath samples (¹⁴CO₂) and indirect calorimetry (energy expenditure) measures were collected at each time point.

Figure 2

Postprandial (6hr) responses in pre- (n=23) and postmenopausal (n=22) women or postmenopausal women (n=12) treated with and without 2 weeks of estradiol for: total serum triglycerides (panels A and B); large buoyant (Sf>400; primarily chylomicron) triglyceride rich lipoprotein (TRL) particles (panels C and D); and medium (Sf 20–400; primarily VLDL).) TRL particles (panels E and F). P-value for group difference in area under the curve.

Figure 3

Postprandial (6hr) responses in pre- (n=23) and postmenopausal (n=22) women or postmenopausal women (n=12) treated with and without 2 weeks of estradiol for: plasma glucose (panels A and B); insulin (panels C and D); and free fatty acids (panels E and F). P-value for group difference in area under the curve.

Figure 4

Twenty four hour energy expenditure (panels A and B), postprandial fat oxidation (panels C and D) and carbohydrate (CHO) oxidation (panels E and F) in pre- (n=23) and postmenopausal (n=22) women or postmenopausal women (n=12) treated with and without 2 weeks of estradiol. P-value for group difference in area under the curve.