“…Podocytes from patients with chronic kidney disease contain lipid droplets that store excess fat (Herman-Edelstein et al, 2014; Kimmelstiel and Wilson, 1936), these cause lipotoxicity by disrupting the mitochondria, as well as endocytosis (Lubojemska et al, 2021), a process crucial to the kidney filtration structure (Wang et al, 2021). Studies in rats and mice on a HFD have repeatedly shown that the animals suffer from obesity, diabetes (altered insulin homeostasis), and kidney injury marked by functional (albuminuria; blood accumulation of BUN and creatinine; increased urinary biomarkers of kidney damage) and structural (glomerulopathy with glomerular hypertrophy and focal segmental glomerulosclerosis; fibrosis) deficiencies (Altunkaynak et al, 2008; Ha et al, 2022; Jiang et al, 2005; Kuwahara et al, 2016; Lu et al, 2003; Rangel Silvares et al, 2019; Ruggiero et al, 2011; Sánchez-Navarro et al, 2021; Sun et al, 2020; Szeto et al, 2016; van der Heijden et al, 2015). Like in patients with chronic kidney disease, lipid droplets have been observed in the kidneys of HFD rats and mice (Deji et al, 2009; Jiang et al, 2005; Sun et al, 2020; van der Heijden et al, 2015) and have been associated with dysfunctional cellular systems including oxidative stress, renal inflammation, ER-stress, disruption of mitochondrial dynamics, and impaired autophagy-lysosomal pathway in the cells of the kidneys (Cai et al, 2024; Ha et al, 2022; Kuwahara et al, 2016; C. Li et al, 2016; Lu et al, 2003; Rangel Silvares et al, 2019; Ruggiero et al, 2011; Sánchez-Navarro et al, 2021; Sun et al, 2020; Szeto et al, 2016; van der Heijden et al, 2015).…”