Nutrients, Volume 18, Issue 13
2026 July-1 - 177 articles
Cover Story: Obesity-associated non-alcoholic fatty liver disease (NAFLD) drives systemic metabolic stress and accelerates chronic kidney disease; yet, the mechanisms linking these conditions remain unclear. Using female Zucker rats, we found that obesity disrupted renal mitochondrial function, increasing ATP despite impaired electron transport and shifting mitochondrial dynamics toward fragmentation. ATPase inhibitory factor 1 (IF1), a regulator of ATP synthase, remained unchanged, suggesting limited adaptation to chronic metabolic stress. Although metformin partially improved mitochondrial bioenergetics, abnormalities persisted. These findings identify renal mitochondrial dysfunction as a mechanistic link between obesity-associated NAFLD and kidney injury, highlighting the need for therapies restoring mitochondrial health beyond metabolic control. View this paper - Issues are regarded as officially published after their release is announced to the table of contents alert mailing list .
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