Acrylamide and Potential Risk of Diabetes Mellitus: Effects on Human Population, Glucose Metabolism and Beta-Cell Toxicity

Abstract

Diabetes mellitus is a frequent endocrine disorder characterized by hyperglycemia. Acrylamide (AA) is food contaminant formed during the high-temperature processing of food rich in carbohydrates and low in proteins. Recent human epidemiological studies have shown a potential association between AA exposure and the prevalence of diabetes in the general population. In male rats, AA treatment promoted pancreatic islet remodeling, which was determined by alpha-cell expansion and beta-cell reduction, while in female rats AA caused hyperglycemia and histopathological changes in pancreatic islets. In vitro and in vivo rodent model systems have revealed that AA induces oxidative stress in beta cells and that AA impairs glucose metabolism and the insulin signaling pathway. Animal studies have shown that diabetic rodents are more sensitive to acrylamide and that AA aggravates the diabetic state. In this review, we provide an overview of human epidemiological studies that examined the relation between AA exposure and glucose disorders. In addition, the effects of AA treatment on pancreatic islet structure, beta-cell function and glucose metabolism in animal models are comprehensively analyzed with an emphasis on sex-related responses. Furthermore, oxidative stress as a putative mechanism of AA-induced toxicity in beta cells is explored. Finally, we discuss the effects of AA on diabetics in a rodent model system.

Protective Effects of Wine Polyphenols on Oxidative Stress and Hepatotoxicity Induced by Acrylamide in Rats

“…GSH is the main cellular antioxidant and one of the most important parameters for assessing oxidative damage [ 25 , 33 ]. The antioxidant effects of wines were demonstrated by the results obtained for the two parameters, reduced GSH and reduced GSH/total GSH ratio, in animal plasma.…”

“…Acrylamide (ACR) is a chemical contaminant that naturally forms during heat processing, at temperatures above 120 °C, by frying, roasting, toasting, grilling or baking of foods rich in carbohydrates and low in proteins [ 20 , 21 , 22 , 23 , 24 , 25 ]. It is abundant in fried and roasted potato, vegetable crisps, cocoa and roasted coffee, bread and pastry, cookies, as well as in tobacco smoke, and, in lower concentrations, in breakfast cereals, biscuits, crackers, roasted nuts, homemade food, human breast milk, infant milk powder and a range of baby foods [ 21 , 23 , 25 , 26 , 27 ].…”

“…Acrylamide (ACR) is a chemical contaminant that naturally forms during heat processing, at temperatures above 120 °C, by frying, roasting, toasting, grilling or baking of foods rich in carbohydrates and low in proteins [ 20 , 21 , 22 , 23 , 24 , 25 ]. It is abundant in fried and roasted potato, vegetable crisps, cocoa and roasted coffee, bread and pastry, cookies, as well as in tobacco smoke, and, in lower concentrations, in breakfast cereals, biscuits, crackers, roasted nuts, homemade food, human breast milk, infant milk powder and a range of baby foods [ 21 , 23 , 25 , 26 , 27 ]. ACR can be absorbed through the digestive tract, respiratory system or through the skin and after exposure can be rapidly distributed to many tissues and organs, such as the thymus, thyroid, liver, heart, brain, spleen, kidneys, as well as the human placenta and breast milk [ 21 , 25 , 27 , 28 ].…”

“…In this context, Regulatory Agencies have provided recommendations for reducing the formation of ACR in food, without setting mandatory limits for maximum acceptable levels of AA in food [ 25 ]. Among the recommendations made by the Spanish Agency for Consumer Affairs, Food Safety, and Nutrition (AECOSAN), in 2015, are: cooking food in the microwave or baking instead of frying, reducing the time and temperature of frying food (<175 °C) and avoiding reuse of frying oil [ 25 ]. At European Union level, “Commission Regulation (EU) 2017/2158” was issued in 2017, setting mitigation measures and benchmark levels to reduce the presence of AA in food [ 32 ].…”

“…Oxidative stress is one of the main mechanisms explaining the neurotoxicity and hepatotoxicity following ACR exposure [ 28 , 30 ]. Increased ROS production, as a result of ACR exposure, may adversely affect cell survival, due to cell membrane damage by oxidative degradation of lipids, proteins, and irreversible DNA modification [ 21 , 25 , 33 ]. Lipid peroxidation, estimated through the level of substances reacting with thiobarbituric acid and of hydroperoxides, as well as products of proteins’ oxidation, such as carbonylated proteins, are markers of oxidative degradation produced by ROS [ 33 ].…”