Beta Cell Dysfunction in Youth- and Adult-Onset Type 2 Diabetes: An Extensive Narrative Review with a Special Focus on the Role of Nutrients

• Published in: Nutrients Vol. 15; no. 9; p. 2217
• Main Authors: Serbis, Anastasios, Giapros, Vasileios, Tsamis, Konstantinos, Balomenou, Foteini, Galli-Tsinopoulou, Assimina, Siomou, Ekaterini
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 07-05-2023; MDPI
• Subjects: Adenosine triphosphate; Adipose tissue; adolescents; Adult; Adults; Age of Onset; Animals; Beta cells; Complications; COVID-19; Diabetes; Diabetes mellitus; Diabetes mellitus (non-insulin dependent); Diabetes Mellitus, Type 2 - diagnosis; Diabetes Mellitus, Type 2 - diet therapy; Diabetes Mellitus, Type 2 - genetics; Diabetes Mellitus, Type 2 - metabolism; Dietary minerals; Epigenesis, Genetic; Failure rates; Fatty acids; Food quality; Glucagon; Glucose; Humans; Insulin; Insulin - biosynthesis; Insulin glargine; Insulin resistance; Insulin secretion; Insulin-Secreting Cells - metabolism; Metabolism; Micronutrients; Minority & ethnic groups; Nutrients; Nutrients - therapeutic use; Obesity; Pancreatic beta cells; Pathogenesis; Pediatrics; Peptides; Prediabetic state; Review; Risk Factors; Teenagers; Type 2 diabetes; Vitamins; Young adults; Youth; β-cell failure; United States > US; β-cell failure; type 2 diabetes; insulin; adolescents; young adults; youth
• ISSN: 2072-6643; 2072-6643
• DOI: 10.3390/nu15092217

Traditionally a disease of adults, type 2 diabetes (T2D) has been increasingly diagnosed in youth, particularly among adolescents and young adults of minority ethnic groups. Especially, during the recent COVID-19 pandemic, obesity and prediabetes have surged not only in minority ethnic groups but also in the general population, further raising T2D risk. Regarding its pathogenesis, a gradually increasing insulin resistance due to central adiposity combined with a progressively defective β-cell function are the main culprits. Especially in youth-onset T2D, a rapid β-cell activity decline has been observed, leading to higher treatment failure rates, and early complications. In addition, it is well established that both the quantity and quality of food ingested by individuals play a key role in T2D pathogenesis. A chronic imbalance between caloric intake and expenditure together with impaired micronutrient intake can lead to obesity and insulin resistance on one hand, and β-cell failure and defective insulin production on the other. This review summarizes our evolving understanding of the pathophysiological mechanisms involved in defective insulin secretion by the pancreatic islets in youth- and adult-onset T2D and, further, of the role various micronutrients play in these pathomechanisms. This knowledge is essential if we are to curtail the serious long-term complications of T2D both in pediatric and adult populations.