Pancreatic α‐cell mass in obesity

• Published in: Diabetes, obesity & metabolism obesity & metabolism, 2017-12, Vol.19 (12), p.1810-1813
• Main Authors: Ellenbroek, Johanne H., Töns, Hendrica A. M., Hanegraaf, Maaike A. J., Rabelink, Ton J., Engelse, Marten A., Carlotti, Françoise, de Koning, Eelco J. P.
• Format: Article
• Language: English
• Subjects: Adaptation; Body Mass Index; Cell Count; Cell Proliferation; Cell Size; Diabetes; Diabetes mellitus; Diabetes mellitus (non-insulin dependent); glucagon; Glucagon - metabolism; Glucagon-Secreting Cells - metabolism; Glucagon-Secreting Cells - pathology; Humans; Image Processing, Computer-Assisted; Immunohistochemistry; Insulin; Insulin - metabolism; Insulin secretion; Insulin-Secreting Cells - metabolism; Insulin-Secreting Cells - pathology; islets; Ki-67 Antigen - metabolism; Middle Aged; Obesity; Obesity - metabolism; Obesity - pathology; Observational studies; observational study; Organ Size; Pancreas; Reproducibility of Results; Secretion; Tissue Donors; β cell
• ISSN: 1462-8902; 1463-1326
• DOI: 10.1111/dom.12997

While it is well recognized that obesity is associated with an increased β‐cell mass, the association with α‐cell mass is less clear. Type 2 diabetes (T2DM) associated with obesity is a bihormonal disease characterized by inadequate insulin secretion and hyperglucagonaemia. We examined β‐ and α‐cell mass throughout the pancreas in obese and lean subjects. Pancreatic tissue of the head, body and tail region of the pancreas was examined from 15 obese subjects (body mass index [BMI] ≥ 27 kg/m2) and 15 age‐matched lean subjects (BMI ≤ 25 kg/m2) without diabetes. In obese subjects both β‐ and α‐cell mass were proportionally higher compared with lean subjects, thereby maintaining the α‐ to β‐cell ratio. The adaptation to obesity occurred preferentially in the head of the pancreas. As data so far have been derived from histological studies of β‐ and α‐cell adaptation, in which the head region of the human pancreas was not included, the adaptive capacity of humans to obesity has previously been underestimated. Obesity is associated with an increased α‐cell mass, which could contribute to the hyperglucagonaemia observed in people with T2DM.