On the one hand, H 2 S increases glucose uptake and fat production in adipocytes, for example: (1) in 3T3L1 adipocytes, H 2 S improves high glucose-induced insulin resistance by up-regulating phosphatidylinositol 3,4,5-trisphosphate level, (2) in diabetic insulin resistance rats, NaHS and H 2 S gas solution improve insulin resistance by activating insulin receptors (IR), (3) CSE/H 2 S converts glucose into triglycerides in adipocytes through peroxisome proliferator-activated receptor (PPAR) and stores them in cells, (4) H 2 S promotes adipogenesis in 3T3L1 cells by increasing the expression of fatty acid protein 4 (8386)
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As these processes intensify, NAD stores are gradually depleted
The pathogenetic role of oxidative stress in NALFD is well known and would explain the rationale for the use of GSH as a potential therapy
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