Journal of Nutrition and Metabolism / 2012 / Article / Tab 1

Review Article

NAFLD, Estrogens, and Physical Exercise: The Animal Model

Table 1

Summary of the central and intrahepatic effects resulting in liver fat accumulation with estrogens withdrawal.

Central effectsIntra-hepatic effects

CNS/hypothalamic effects Lipid uptake
(i) ↑ Food consumption
(ii)↑ Leptin secretion
(iii) Activity and energy expenditure
(i) Unknown (possible mechanism of upregulation of fatty acid uptake via estrogens-dependent pathways, yet to be explored)

Lipid profile and adipose tissue effects Lipogenesis
(i) Absence of estrogens causes fat redistribution/gain particularly increased intra-abdominal fat and altered lipid homeostasis (portal/fatty acid flux theory)(i) SREBP-1c and PGC1α
(ii) SCD-1
(iii) FAS
(iv) ACC
(v) PPAR-γ
Lipid oxidation
(i) PPAR-α
(ii) HSL
(iii) Fatty acid β-oxidation
VLDL-TG production and secretion system
(i) VLDL-TG production in Ovx rats
(ii) MTP and DGAT2

CNS: central nervous system; SREBP-1c: sterol-regulatory-element-binding-protein 1c; PGC1α: peroxisome proliferator-activated receptor gamma coactivator-1 alpha; SCD-1: stearoyl-CoA desaturase-1; FAS: fatty acid synthase; ACC: acetyl-CoA carboxylase; PPAR-α, -γ: peroxysome proliferator-activated receptor-alpha, -gamma; HSL: hormone-sensitive lipase; VLDL-TG: very low density lipoprotein-triglyceride; MTP: microsomal triglyceride transfer protein; DGAT2: diacyl-glycerol acyltransferase-2.

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