Dietary Acrylamide-Glycidamide Exposure and Metabolic Toxicity: Emerging Evidence in Type 2 Diabetes

Acrylamide is present in a variety of cooked and processed foods, but its precise role in the biological mechanisms underlying type 2 diabetes (T2D) remains incompletely understood. This review aimed to comprehensively evaluate the relationship between dietary acrylamide exposure, T2D-related metabolic dysfunction, and the molecular mechanisms responsible for its adverse effects.

A narrative literature review was conducted by searching PubMed®, ScienceDirect®, Google Scholar®, and MEDLINE® for English-language publications published between 2002 and 2025. The search strategy used the following Boolean search string: ("acrylamide" OR "glycidamide") AND ("diabetes" OR "type 2 diabetes" OR "insulin resistance" OR "β-cell dysfunction") AND ("oxidative stress" OR "glucose metabolism"). More than 100 relevant publications were identified and included in this review.

Current evidence suggests that dietary acrylamide exposure contributes to metabolic dysfunction through multiple interconnected mechanisms, including oxidative stress, chronic inflammation, glycation, insulin resistance, and pancreatic β-cell dysfunction. Experimental and epidemiological studies indicate that acrylamide may impair glucose metabolism and insulin signalling, thereby contributing to the development and progression of T2D. However, the consistency of epidemiological evidence remains limited by methodological differences and potential confounding factors.

The available evidence highlights the potential role of dietary acrylamide as a modifiable environmental risk factor for T2D. Strategies aimed at reducing dietary acrylamide exposure through improved food processing, cooking practices, and nutritional interventions may help mitigate metabolic risk. Nevertheless, further well-designed prospective studies and mechanistic investigations are needed to clarify the causal relationship and strengthen the current evidence base.

Dietary acrylamide exposure may adversely affect glucose homeostasis, insulin sensitivity, and pancreatic β-cell function, thereby contributing to the development and progression of T2D. Although current evidence supports a potential association, further high-quality clinical and epidemiological studies are required to establish causality and inform evidence-based preventive strategies.