Samantha B. J. Schipper, Maaike M. Van Veen, Petra J. M. Elders, Annemieke van Straten, Ysbrand D. Van Der Werf, Kristen L. Knutson, Femke Rutters
Sleep disorders are linked to type 2 diabetes and diabetes complications. In this issue, Schipper et al (https://doi.org/10.1007/s00125-021-05541-0) summarise the evidence demonstrating a high prevalence of sleep disorders in type 2 diabetes compared with the general population. They also discuss the association between sleep disorders and health outcomes, such as glycaemic control, microvascular and macrovascular complications, depression, mortality and quality of life. Additionally, they show that treating sleep disorders in people with type 2 diabetes improves these aforementioned health outcomes. The authors conclude that efforts should, therefore, be made to diagnose and treat sleep disorders in people with type 2 diabetes in order to ultimately improve their health and quality of life. The figures from this review are available as a downloadable slideset.
Matthew A. Budd, Mahdis Monajemi, Sarah J. Colpitts, Sarah Q. Crome, C. Bruce Verchere, Megan K. Levings
Regulatory immune cells are known to control both innate and adaptive immunity, mitigating autoreactivity in type 1 diabetes. However, simply preventing autoimmune attack may not be sufficient to restore the function of damaged or destroyed islet beta cells. In this issue, Budd, Monajemi and Colpitts, et al (https://doi.org/10.1007/s00125-021-05565-6) summarise evidence suggesting that regulatory immune cells may also mediate tissue repair and regeneration, thus working to restore beta cell function. Focussing on macrophages, innate lymphoid cells and regulatory T cells, the authors discuss possible regenerative mechanisms of action and how networks of regulatory cells may work together to enhance beta cell function. They also highlight how technological advances will further knowledge in this area, potentially enabling new therapeutic avenues for type 1 diabetes. The figure from this review is available as a downloadable slide.
Yi-Xin Wang, Siwen Wang, Makiko Mitsunami, JoAnn E. Manson, Janet W. Rich-Edwards, Liang Wang, Cuilin Zhang, Jorge E. Chavarro
Long or irregular menstrual cycles have been associated with many endocrine-related diseases, but evidence linking menstrual cycle dysfunction with gestational diabetes mellitus is scant. In this issue, Wang et al (https://doi.org/10.1007/s00125-021-05531-2) report that, among 10,906 premenopausal women participating in the Nurses’ Health Study II, both irregular and long menstrual cycles during mid-adulthood (age 29–46 years) are associated with a greater risk of gestational diabetes mellitus. These associations are independent of BMI determined across the reproductive lifespan, as well as other well-known risk factors for gestational diabetes mellitus (e.g. advanced maternal age, greater parity and unhealthy lifestyles). The authors conclude that these findings indicate that menstrual cycle characteristics before pregnancy may serve as early markers for subsequent risk of gestational diabetes mellitus.
Jiangbo Du, Jiong Li, Xiaoqin Liu, Hu Liu, Carsten Obel, Hongbing Shen, Zhibin Hu, Yongfu Yu
Intrauterine exposure to high levels of glucose may lead to vision impairment in offspring. However, whether, or to what extent, prenatal exposure to maternal diabetes increases the risk of refractive error (RE) in offspring is still unknown. In this issue, Du and Li, et al (https://doi.org/10.1007/s00125-021-05526-z) report that children of mothers with diabetes, especially those mothers with diabetic compilations, have increased risk of developing high RE in general, as well as specific types of high RE, persisting from the neonatal period to early adulthood. The authors conclude that these findings highlight the importance of early ophthalmological screening in children of mothers with diabetes diagnosed before or during pregnancy.
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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