Table 1: Drugs used in dyslipidemia: classical effects, effects on adipose tissue, and weight.

Drugs used in dyslipidemiaClassical mechanism of actionAdipose tissue effectsWeight
AT mass/AT depotsGlucose metabolism/insulin sensitivityLipid metabolismAdipokine expressionAntiatherogenicAdipogenesisBrowning effectAnti-inflammatory

Statins⊝ HMG -CoA reductase enzyme↓ EAT [63]⊝ caveolae dysfunction [89];
⊝ GLUT4 expression and translocation [95]; NLRP3 inflammasome activation [195];
⊕ ↑ SIRT1 and PGC-1α leading to PPARγ and GLUT4 [9799]; modulation of adipokine expression [83, 97]
⊕ lipolysis [62]
↓ lipid accumulation (⊕ LPL) [64, 65]
⊕ lipogenesis and ↑ lipid accumulation [196]
Adiponectin [62, 67, 68, 73, 76, 80]Leptin [6771]; resistin [67, 72, 73]; IL-6 [67, 7478]; PAI-1 [7981]; MCP-1 [77, 78, 80, 82, 83]; visfatin [71] and TNFα [67, 68, 71, 77, 82, 83]⊕ PPARγ and SRBI expression (adipocyte uptake of oxLDL) [88, 90];
vide adipokine expression modulation
⊝ [66, 101103]
in vivo [107, 108]
⊝ ER stress [82];
⊕ iNOS expression [75, 85]
— [98, 99]
FibratesPPARα agonists⊕ [115, 122]↓ [114, 117120, 124, 125]
BezafibrateNonselective⊕ FA oxidation [113115]
⊝ lipogenesis [113]
Adiponectin [130, 131]TNFα [130, 131]⊕ UCP-1, 2, and 3 expression [113, 114]
GemfibrozilSelective⊕ lipogenesis [116]
FenofibrateSelective↓ VAT [125]⊕ [119, 120, 125]⊕ FA oxidation [118, 119]
⊝ lipogenesis [121]
Adiponectin [67, 126]; vaspin [124]MCP1 [127]; TNFα [67, 125, 127, 128]; leptin [120, 125]⊕ oxLDL uptake [134]
⊕ CD36 expression [134]
⊕ [117, 120]⊝ CD40 expression (AMPK pathway) [132]
⊝ AOX1 expression [133]
↓ [117120, 125]
Ezetimibe⊝ NPC1L1 transporter↓ VAT [155]⊕ [155]Adiponectin [155]Visfatin [156]— [155]
Niacin⊝ HDL-apoA-I holoparticle receptor in hepatocytes⊝ [148, 151]⊕ lipolysis [144146]
⊝ lipogenesis
Adiponectin [145]; leptin (chronic treatment) [151]MCP1, RANTES, fractalkine [150]↑ n-3 PUFAs and its metabolites [149];
⊕ HDL-induced cholesterol efflux from adipocytes; ↑ HDL levels [140, 152]
⊕ [154]Vide adipokine effects

⊕: stimulates; ⊝: inhibits; —: without effect; AT: adipose tissue; TG: triglycerides; HMG-CoA: 3-hydroxy-3-methyl-glutaryl-coenzyme A; GLUT4: glucose transporter type 4; NLRP3: NOD-like receptor family, pyrin domain containing 3; SIRT1: sirtuin 1; PPARs: peroxisome proliferator-activated receptors; PGC-1α: peroxisome proliferator-activated receptor γ coactivator 1 alpha; LPL: lipoprotein lipase; TNFα: tumour necrosis factor α; IL: interleukin; CCL2 or MCP-1: CC-chemokine ligand 2; PAI-1: plasminogen activator inhibitor type 1; SRB1: scavenger receptor 1; oxLDL: oxidized LDL; CD36/FAT: fatty acid translocase; ER: endoplasmic reticulum; iNOS: inducible nitric oxide synthase; UCP: uncoupling protein; NPC1L1: Niemann-Pick C1-Like 1; VAT: visceral AT; FA: fatty acid; AMPK: adenosine monophosphate-activated protein kinase; AOX1: aldehyde oxidase 1; CD40: cluster of differentiation 40; sICAM-1: soluble intracellular adhesion molecule-1; HDLs: high-density lipoproteins; PUFAs: n-3 polyunsaturated fatty acids.