Depleting hypothalamic somatostatinergic neurons recapitulates diabetic phenotypes in mouse brain, bone marrow, adipose and retina – published online 24/08/2021

Chao Huang, Robert F. Rosencrans, Raluca Bugescu, Cristiano P. Vieira, Ping Hu, Yvonne Adu-Agyeiwaah, Karen L. Gamble, Ana Leda F. Longhini, Patrick M. Fuller, Gina M. Leinninger, Maria B. Grant

Low grade inflammation and an increased number of circulating monocytes are key features of diabetes that exacerbate many diabetic complications, including diabetic retinopathy. In this issue, Huang and Rosencrans, et al (https://doi.org/10.1007/s00125-021-05549-6) report that, in mice, a type 2 diabetes-associated loss of hypothalamic somatostatin is sufficient to induce neuroinflammation and bias haematopoiesis towards a proinflammatory monocyte phenotype without overtly altering glucose homeostasis. The authors conclude that these findings provide evidence that neuroinflammation is sufficient to initiate several diabetic complications. This supports the repurposing of somatostatin analogues, such as octreotide, for management of neuroinflammation in diabetes.

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