Tier 3 — preclinical

Fisetin averts oxidative stress in pancreatic tissues of streptozotocin-induced diabetic rats

Prasath GS, Sundaram CS, Subramanian SP
Endocrine 2013 44(2):359-68

Bibliography

PubMed
PMID 23277230
Funding
Not explicitly stated in the reviewed sections; conducted at the Department of Biochemistry, University of Madras.
Competing interests
Not stated in the reviewed sections.

Study snapshot

DesignStreptozotocin (STZ, 50 mg/kg i.p.)-induced diabetic rat model, oral fisetin (10 mg/kg/day, 30 days), with blood glucose, HbA1c, plasma insulin, pancreatic and plasma antioxidant status, NF-kB p65 and IL-1beta measurement, plus in vitro DPPH/ABTS radical-scavenging assays and pancreatic histology.
ModelMale Wistar rats, streptozotocin-induced experimental diabetes.
SampleNot stated in the reviewed abstract/sections beyond group-level design; gliclazide used as an active comparator.
InterventionFisetin 10 mg/kg body weight, oral, once daily for 30 days, versus gliclazide comparator and untreated diabetic controls.
Duration30 days.
EndpointsBlood glucose and glycosylated haemoglobin (HbA1c); Plasma insulin; Pancreatic NF-kB p65 and plasma IL-1beta; Serum nitric oxide; Antioxidant status in pancreas and plasma; DPPH and ABTS free-radical scavenging activity (in vitro); Pancreatic histology

What the study showed, in plain terms

Chronic high blood sugar drives oxidative stress that damages the insulin-producing pancreas, so this study tested whether fisetin — already shown to lower blood glucose in this same rat model — could also protect pancreatic tissue from that oxidative damage.

Researchers at the University of Madras gave streptozotocin-diabetic rats oral fisetin for 30 days and measured blood sugar control alongside antioxidant status and inflammatory markers in the pancreas.

Fisetin significantly lowered blood glucose, HbA1c, pancreatic NF-kB p65 and plasma IL-1beta, while improving antioxidant status in both pancreas and plasma; standalone assays confirmed fisetin's direct free-radical scavenging activity, and pancreatic tissue looked structurally better preserved on histology.

Bottom line: a rat study supporting fisetin's antioxidant and anti-inflammatory action in the diabetic pancreas, on top of its glucose-lowering effect — but it's rodent data using a chemically-induced diabetes model, not evidence from people with type 2 diabetes.

Key findings

Oral fisetin (10 mg/kg/day, 30 days) significantly reduced blood glucose, HbA1c, pancreatic NF-kB p65 and plasma IL-1beta in streptozotocin-diabetic rats, improved antioxidant status in pancreas and plasma, and preserved pancreatic histology; in vitro assays confirmed fisetin's direct free-radical scavenging (DPPH, ABTS) activity.

What this study can and cannot tell us

Streptozotocin-induced diabetes is a chemically-induced rodent model that mimics some but not all features of human type 1/type 2 diabetes. Single 10 mg/kg dose tested; no dose-response data. No human data, and gliclazide (a sulfonylurea) is a partial rather than mechanistic comparator for fisetin's antioxidant claims.

Editorial review

Reviewed by the Biohack Blueprint research team

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