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<p>Inflammasome activation, particularly through the NLRP3 complex, plays a central role in the progression of diabetes mellitus and its major co-morbidities, including nephropathy, neuropathy, retinopathy, cardiovascular dysfunction, and metabolic liver disease. This systematic review aimed to synthesise contemporary evidence on inflammasome signalling mechanisms in diabetes and its complications and the modulatory effects of dietary phytochemicals and nutraceuticals on these pathways. Following PRISMA guidelines, a systematic search was conducted across PubMed (n = 158), Scopus (n = 144), Web of Science (n = 126), and Google Scholar (n = 180) from inception to July 2025. Preclinical in vivo studies (rodent models of type 1 and type 2 diabetes, high-fat diet models, STZ—and alloxan-induced models), in vitro experiments (pancreatic β-cells, hepatocytes, renal and vascular cells), and a limited number of clinical studies evaluating circulating inflammasome markers in human diabetic cohorts. Study selection followed PRISMA guidelines, and only studies reporting explicit NLRP3, ASC, caspase-1, IL-1β or IL-18 outcomes were included. A total of 139 studies were included. Diabetes consistently generated NLRP3 inflammasome activation across models via hyperglycaemia-driven oxidative stress, mitochondrial dysfunction, TXNIP up-regulation, and lipid-mediated metabolic stress. Phytochemicals such as curcumin, quercetin, resveratrol, berberine, sulforaphane, and flavonoid-rich extracts exhibited inhibitory effects on these pathways by diminishing ROS generation, inhibiting NF-κB priming, augmenting AMPK signaling, preserving mitochondrial integrity, and downregulating downstream IL-1β/IL-18 release. Data from several organ systems indicates a uniform trend of inflammasome inhibition and enhanced metabolic or vascular results. Available literature indicates that phytochemicals exert reproducible, mechanistically coherent inhibition of NLRP3 inflammasome activation in both preclinical and limited clinical settings. These findings highlight the therapeutic potential of dietary bioactives as adjunct modulators of inflammation-driven diabetic complications.</p>

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A systematic review of inflammasome signalling, diabetes co-morbidities and nutraceuticals: a three-fold cord that can be dietarily broken

  • 期刊论文

  • 发表日期：

    2026年4月10日

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  • Bayo Olufunso Adeoye,
  • Oyedayo Phillips Akano,
  • Oluwatoyin Michael Daniyan,
  • Peace Awele Mokogwu,
  • Adedayo Hakeem Oyebanji,
  • Modupe Olusola Adetayo,
  • Oludayo Adeyemi Olosunde,
  • Ayodeji David Adeoye,
  • Sandra Onyinyechi Ajaere,
  • Opeyemi Adebola Adetunji,
  • Oluwaseun Adetayo Adewole

摘要

Inflammasome activation, particularly through the NLRP3 complex, plays a central role in the progression of diabetes mellitus and its major co-morbidities, including nephropathy, neuropathy, retinopathy, cardiovascular dysfunction, and metabolic liver disease. This systematic review aimed to synthesise contemporary evidence on inflammasome signalling mechanisms in diabetes and its complications and the modulatory effects of dietary phytochemicals and nutraceuticals on these pathways. Following PRISMA guidelines, a systematic search was conducted across PubMed (n = 158), Scopus (n = 144), Web of Science (n = 126), and Google Scholar (n = 180) from inception to July 2025. Preclinical in vivo studies (rodent models of type 1 and type 2 diabetes, high-fat diet models, STZ—and alloxan-induced models), in vitro experiments (pancreatic β-cells, hepatocytes, renal and vascular cells), and a limited number of clinical studies evaluating circulating inflammasome markers in human diabetic cohorts. Study selection followed PRISMA guidelines, and only studies reporting explicit NLRP3, ASC, caspase-1, IL-1β or IL-18 outcomes were included. A total of 139 studies were included. Diabetes consistently generated NLRP3 inflammasome activation across models via hyperglycaemia-driven oxidative stress, mitochondrial dysfunction, TXNIP up-regulation, and lipid-mediated metabolic stress. Phytochemicals such as curcumin, quercetin, resveratrol, berberine, sulforaphane, and flavonoid-rich extracts exhibited inhibitory effects on these pathways by diminishing ROS generation, inhibiting NF-κB priming, augmenting AMPK signaling, preserving mitochondrial integrity, and downregulating downstream IL-1β/IL-18 release. Data from several organ systems indicates a uniform trend of inflammasome inhibition and enhanced metabolic or vascular results. Available literature indicates that phytochemicals exert reproducible, mechanistically coherent inhibition of NLRP3 inflammasome activation in both preclinical and limited clinical settings. These findings highlight the therapeutic potential of dietary bioactives as adjunct modulators of inflammation-driven diabetic complications.