Misregulation of PPAR Functioning and Its Pathogenic Consequences Associated with Nonalcoholic Fatty Liver Disease in Human Obesity

<table>Obesity-induced liver oxidative stress (A), hypoadiponectinemia (B), and endoplasmic reticulum stress (C) as factors leading to hepatic steatosis in nonalcoholic fatty liver disease. <i>Abbreviations: </i><svg height="11.425" id="M3" style="vertical-align:-0.0pt" version="1.1" viewbox="0 0 11.025 11.425" width="11.025" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink">
<g transform="matrix(.017,-0,0,-.017,.062,11.363)"><path d="M600 0h-557v24l268 633l28 8l261 -641v-24zM497 50l-194 489l-196 -489h390z" id="x394"></path></g>
</svg>5(6)D: delta-5(6) desaturase; FA, fatty acid; LCPUFA: long-chain polyunsaturated fatty acid; PPAR-<i>α</i>(<i>γ</i>): peroxisome proliferator-activated receptor-<i>α</i>(<i>γ</i>); SREBP-1c: sterol regulatory element binding protein-1c; UPR: unfolded protein response.</table>

PPAR Research

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Figure 1

Figure 1: Misregulation of PPAR Functioning and Its Pathogenic Consequences Associated with Nonalcoholic Fatty Liver Disease in Human Obesity 