, Volume 60, Issue 7, pp 1161–1162

Up front

Up front

DOI: 10.1007/s00125-017-4311-6

Cite this article as:
Diabetologia (2017) 60: 1161. doi:10.1007/s00125-017-4311-6

Diabetes, bone and glucose-lowering agents: basic biology

Beata Lecka-Czernik

Bone fragility is a known pathological complication of diabetes. In this issue, Beata Lecka-Czernik (DOI 10.1007/s00125-017-4269-4) summarises basic research findings on the aetiology of increased fracture risk in both type 1 and type 2 diabetes. Diminished bone quality in diabetes is associated with attenuated bone remodelling. Multiple mechanisms contribute to diabetic bone syndrome including impairments in glucose metabolism, microvasculature and muscle endocrine function, as well as an accumulation of advanced glycation end-products (AGEs). In addition, bone is a target for several glucose-lowering therapies, providing additional support for the concept that bone is an integral part of energy metabolism and that the bone safety of treatments for diabetes needs to be considered.

Diabetes, bone and glucose-lowering agents: clinical outcomes

Ann V. Schwartz

Fracture prevention is an important clinical goal in older adults with type 2 diabetes. Fracture risk is higher and, when a fracture does occur, recovery is more difficult in those with diabetes. In this issue, a review by Ann Schwartz (DOI 10.1007/s00125-017-4283-6) focuses on our understanding of key clinical considerations in the management of fracture risk in diabetes: fracture risk assessment, skeletal effects of glucose-lowering medications, and the effectiveness of standard approaches to fracture prevention in those with diabetes. Standard tools for fracture risk assessment, bone mineral density T-score and FRAX, are useful in older adults with diabetes but tend to underestimate risk. Diabetes-specific factors—longer duration, complications and poor glycaemic control—contribute to increased risk. Glucose-lowering medications vary in their effects on the skeleton, an important consideration for those with higher fracture risk. Although evidence is currently limited, standard osteoporosis medications appear to be effective in preventing bone loss and fracture in those with diabetes.

Lipoprotein lipase in hypothalamus is a key regulator of body weight gain and glucose homeostasis in mice

Elise Laperrousaz, Valentine S. Moullé, Raphaël G. Denis, Nadim Kassis, Chloé Berland, Benoit Colsch, Xavier Fioramonti, Erwann Philippe, Amélie Lacombe, Charlotte Vanacker, Noémie Butin, Kimberley D. Bruce, Hong Wang, Yongping Wang, Yuanqing Gao, Cristina Garcia-Caceres, Vincent Prévot, Matthias H. Tschöp, Robert H. Eckel, Hervé Le Stunff, Serge Luquet, Christophe Magnan, Céline Cruciani-Guglielmacci

Brain hydrolysis of triacylglycerol-enriched particles may participate in the control of energy balance. In this issue, Laperrousaz et al (DOI 10.1007/s00125-017-4282-7) demonstrate that lipoprotein lipase (LPL) in the mediobasal hypothalamus (MBH) contributes to the regulation of body weight and glucose homeostasis. Indeed, the partial deletion of Lpl in the MBH in mice leads to an increase in body weight gain compared with controls, associated with early glucose intolerance and lower locomotor activity before any change in body weight. Conversely, MBH-specific overexpression of Lpl induces a decrease in body weight. Interestingly, decreased LPL activity in the hypothalamus is accompanied by a transient drop in ceramide levels, which could mediate the metabolic changes towards anabolism. A better understanding of the implication of hypothalamic lipid metabolism in the regulation of energy homeostasis may potentially provide new therapeutic opportunities.

Hyperglycaemic memory affects the neurovascular unit of the retina in a diabetic mouse model

Patrick Friedrichs, Andrea Schlotterer, Carsten Sticht, Matthias Kolibabka, Paulus Wohlfart, Axel Dietrich, Thomas Linn, Grietje Molema, Hans-Peter Hammes.

After initial periods of hyperglycaemia, subsequent good glycaemic control fails to prevent the development and progression of diabetes complications; this phenomenon is termed hyperglycaemic memory. In this issue Friedrichs et al (DOI 10.1007/s00125-017-4254-y) report on how they established a mouse model of hyperglycaemic memory to study the underlying mechanisms and identify genes involved in the glucose-independent progression of diabetic retinopathy. After confirmation of persistent microvascular damage following blood glucose normalisation, the authors found that cytoskeletal and nuclear genes met the criteria of a memory-like regulation. The functions of these genes suggest the involvement of the entire neurovascular unit. These findings should direct the focus of future studies from cell-type-specific alterations towards disturbances of cell–cell communication within the neurovascular unit.

All text supplied by the authors.

Copyright information

© Springer-Verlag Berlin Heidelberg 2017

Personalised recommendations