FLAXSEED, SEA BUCKTHORN AND CORNELIAN CHERRY IN TYPE 2 DIABETES: GUT MICROBIOTA AND METABOLIC BENEFITS—A NARRATIVE REVIEW

Abstract

Type 2 diabetes mellitus (T2DM) represents over 90% of diabetes cases worldwide and continues to rise in prevalence due to aging populations, sedentary lifestyles, obesity, and nutritional transitions. The disease is characterized by progressive insulin resistance, pancreatic β-cell dysfunction, chronic hyperglycemia, oxidative stress, and low-grade inflammation, leading to multi-organ complications including cardiovascular, renal, neural, and ocular damage. Emerging evidence identifies gut microbiota dysbiosis and metabolic endotoxemia as central contributors to T2DM pathogenesis. Reduced microbial diversity, impaired short-chain fatty acid (SCFA) production, and increased intestinal permeability facilitate lipopolysaccharide (LPS) translocation, triggering inflammatory cascades that may interfere with insulin signaling.

Dietary bioactive compounds capable of modulating gut microbial composition and supporting intestinal barrier integrity have therefore gained attention as adjunctive therapeutic strategies. This review analyzes the mechanistic effects of three phytochemically rich plant sources—flaxseed (Linum usitatissimum), sea buckthorn (Hippophae rhamnoides), and cornelian cherry (Cornus mas) - in the context of T2DM. Flaxseed lignans and fermentable fibre may enhance SCFA production, potentially suppress hepatic gluconeogenesis, and attenuate inflammatory signaling. Sea buckthorn polyphenols may help reshape microbial ecology, activate AMPK-dependent pathways, improve lipid metabolism, and are associated with multi-organ protection. Cornelian cherry iridoids and anthocyanins may modulate antioxidant and inflammatory pathways, contribute to  improved insulin sensitivity, and support vascular and endothelial function.

Collectively, these plant-derived bioactives converge on shared metabolic nodes, including restoration of gut barrier integrity, reduction of metabolic endotoxemia, activation of AMPK signaling, suppression of hepatic glucose production, enhancement of peripheral glucose uptake, and improvement of lipid homeostasis. Targeting the gut–liver–pancreas axis through microbiota-mediated mechanisms may represent a rational adjunctive strategy for mitigating insulin resistance and limiting the progression of T2DM and its complications.