Resveratrol improves lipid metabolism in diabetic nephropathy rats

Zhao, Yong-Qi; Fan, Youjia

doi:10.2741/4885

Cited by 14 publications

(12 citation statements)

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“…In AMD patients, long-term intake of resveratrol-containing supplements provides a broad bilateral improvement in ocular structure and visual function [ 48 ]. It is now quite well established that resveratrol induces autophagy through either AMPK/SIRT1 activation or PI3K/AKT/mTORC1/2 inhibition [ 201 , 202 , 203 , 204 , 205 , 206 , 207 , 208 , 209 , 210 , 211 ]. This is associated with longevity and anti-inflammatory, antioxidant, and anti-apoptotic effects, as well as lipid- and glucose-regulating effects, in a variety of experimental conditions [ 201 , 202 , 203 , 204 , 205 , 206 , 207 , 208 , 209 , 210 , 211 ].…”

Section: Lutein Resveratrol and Vaccinium Myrtillusmentioning

confidence: 99%

“…It is now quite well established that resveratrol induces autophagy through either AMPK/SIRT1 activation or PI3K/AKT/mTORC1/2 inhibition [ 201 , 202 , 203 , 204 , 205 , 206 , 207 , 208 , 209 , 210 , 211 ]. This is associated with longevity and anti-inflammatory, antioxidant, and anti-apoptotic effects, as well as lipid- and glucose-regulating effects, in a variety of experimental conditions [ 201 , 202 , 203 , 204 , 205 , 206 , 207 , 208 , 209 , 210 , 211 ]. Resveratrol-induced autophagy is also associated with the rescue of NRF-2, which is involved in autophagy-related mitophagy and mitochondriogenesis, protection from oxidative stress, and caspase-related apoptosis, as well as downregulation of NF-κB, NLRP3, and pro-inflammatory cytokines production [ 203 , 206 , 207 , 208 , 209 , 210 , 211 ].…”

Section: Lutein Resveratrol and Vaccinium Myrtillusmentioning

confidence: 99%

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A Re-Appraisal of Pathogenic Mechanisms Bridging Wet and Dry Age-Related Macular Degeneration Leads to Reconsider a Role for Phytochemicals

Pinelli

Biagioni

Limanaqi

et al. 2020

IJMS

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Which pathogenic mechanisms underlie age-related macular degeneration (AMD)? Are they different for dry and wet variants, or do they stem from common metabolic alterations? Where shall we look for altered metabolism? Is it the inner choroid, or is it rather the choroid–retinal border? Again, since cell-clearing pathways are crucial to degrade altered proteins, which metabolic system is likely to be the most implicated, and in which cell type? Here we describe the unique clearing activity of the retinal pigment epithelium (RPE) and the relevant role of its autophagy machinery in removing altered debris, thus centering the RPE in the pathogenesis of AMD. The cell-clearing systems within the RPE may act as a kernel to regulate the redox homeostasis and the traffic of multiple proteins and organelles toward either the choroid border or the outer segments of photoreceptors. This is expected to cope with the polarity of various domains within RPE cells, with each one owning a specific metabolic activity. A defective clearance machinery may trigger unconventional solutions to avoid intracellular substrates’ accumulation through unconventional secretions. These components may be deposited between the RPE and Bruch’s membrane, thus generating the drusen, which remains the classic hallmark of AMD. These deposits may rather represent a witness of an abnormal RPE metabolism than a real pathogenic component. The empowerment of cell clearance, antioxidant, anti-inflammatory, and anti-angiogenic activity of the RPE by specific phytochemicals is here discussed.

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Section: Lutein Resveratrol and Vaccinium Myrtillusmentioning

confidence: 99%

Section: Lutein Resveratrol and Vaccinium Myrtillusmentioning

confidence: 99%

A Re-Appraisal of Pathogenic Mechanisms Bridging Wet and Dry Age-Related Macular Degeneration Leads to Reconsider a Role for Phytochemicals

Pinelli

Biagioni

Limanaqi

et al. 2020

IJMS

View full text Add to dashboard Cite

show abstract

“…In models of kidney disease, resveratrol increased AMPK and PGC1a expression and mitigated diabetic nephropathy. 107,111,112 Similarly, resveratrol decreased profibrotic signalling 47 and renal scarring in a mouse folic acid model. 64 In an AKI model, resveratrol reduced severity of toxic injury or IRI 101,102,135 and restored mitochondrial respiratory capacity after hemorrhagic shock.…”

Section: Pgc1a and Kidney Diseasementioning

confidence: 94%

“…110 Increasing PGC1a through overexpression or pharmacologic stimulation of SIRT1 reduced albuminuria in diabetic mice and protected podocytes from glucose-mediated reduction of respiratory complex activity, alterations in mitochondrial membrane potential, and impaired autophagy. 72,107,111,112 Overexpression of PGC1a targets using the PPARg agonist, rosiglitazone, protected diabetic mouse kidneys, and cultured podocytes against oxidative damage and glomerulosclerosis. Analogously, stimulation with metformin or AICAR, (both of which activate AMPK) or resveratrol reduced renal expression of profibrotic TGF-b1 and asmooth muscle actin.…”

Section: Pgc1a and Kidney Diseasementioning

confidence: 99%

“…Analogously, stimulation with metformin or AICAR, (both of which activate AMPK) or resveratrol reduced renal expression of profibrotic TGF-b1 and asmooth muscle actin. 91,92,111,112 There is also evidence from diabetic rats and cultured podocytes that PGC1a expression promoted expression of key podocyte genes-nephrin and podocalyxin-that maintain filtration barrier integrity. 107,113 In a type 2 diabetes mouse model, hyperglycemia also led to accumulation of lipids in diabetic kidneys 114 with resultant lipotoxicity and oxidative stress, which has long been associated with DKD progression.…”

Section: Pgc1a and Kidney Diseasementioning

confidence: 99%

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