Type 1 diabetes: where are we in 2017?

Copenhaver, Melanie M.; Hoffman, Robert R.

doi:10.21037/tp.2017.09.09

Cited by 24 publications

(17 citation statements)

References 43 publications

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“…Increased fracture risk due to diabetic bone disease is increasingly understood to be a burdensome health problem for both type I and type II diabetics. Not only are both type II and type I diabetes on the rise, but with advances in treatments for diabetes, diabetics are living longer lives . It is, therefore, important to develop new approaches to address osteopenia in light of the aging population of diabetic patients to ensure that mobility and quality of life are not further compromised.…”

Section: Discussionmentioning

confidence: 99%

“…Not only are both type II and type I diabetes on the rise, but with advances in treatments for diabetes, diabetics are living longer lives. (48) It is, therefore, important to develop new approaches to address osteopenia in light of the aging population of diabetic patients to ensure that mobility and quality of life are not further compromised. We therefore sought to identify a molecular mechanism for diabetic bone disease using a mouse model for type I diabetes.…”

Section: Discussionmentioning

confidence: 99%

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Impaired Gastric Hormone Regulation of Osteoblasts and Lysyl Oxidase Drives Bone Disease in Diabetes Mellitus

et al. 2019

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Diabetic bone disease is a complication of type I and type II diabetes, both of which are increasing in the United States and elsewhere. Increased hip and foot fracture rates do not correlate well with changes in bone mineral density (BMD), whereas studies support the importance of collagen structure to bone strength. Extracellular lysyl oxidase (LOX) catalyzes the oxidative deamination of hydroxylysine and lysine residues in collagens resulting in aldehydes that subsequently form critically important biosynthetic crosslinks that stabilize functional collagens. Although LOX‐dependent biosynthetic crosslinks in bone collagen are deficient in diabetic bone, the expression and regulation of bone LOXs in diabetes have not been comprehensively studied. Here, we found that LOX is profoundly downregulated in bone in diabetes. Moreover, we have identified a novel metabolic regulatory relationship that is dysregulated in diabetes using mouse models. Data indicate that the incretin (gastric hormone) known as glucose‐dependent insulinotropic polypeptide (GIP) that is anabolic to osteoblasts strongly upregulates LOX, and that this regulation is disrupted in the streptozotocin‐induced model of diabetes in mice. In vivo and in vitro studies support that diabetes results in elevated circulating peripheral dopamine, likely also derived from the gut, and is responsible for blocking GIP signaling and LOX levels in osteoblasts. Moreover, peripheral administration of the dopamine D2 receptor antagonist amisulpride to diabetic mice restored trabecular bone structure to near normal and partially reversed downregulation of LOX. Taken together our data identifies a novel metabolic relationship between the gut‐derived hormone GIP and bone‐derived LOX, and points to the importance of LOX dysregulation in the pathology of diabetic bone disease. © 2019 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of the American Society for Bone and Mineral Research.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Impaired Gastric Hormone Regulation of Osteoblasts and Lysyl Oxidase Drives Bone Disease in Diabetes Mellitus

et al. 2019

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“…Exposure to pathogens can have a profound impact on the health of an individual both directly and through connections with other diseases 1 . Studies have linked infectious agents to autoimmune diseases (such as with multiple sclerosis 2 and type 1 diabetes in children 3 ), cancers 4 , drug hypersensitivity 5 and psychiatric disorders 6 . Investigating early life exposure to specific infectious agents is critical to our understanding of the infectious aetiologies of diseases of interest and the impact that infection may have on development.…”

Section: Introductionmentioning

confidence: 99%

Longitudinal serological measures of common infection in the Avon Longitudinal Study of Parents and Children cohort

et al. 2018

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Antibodies against pathogens provide information on exposure to infectious agents and are meaningful measures of past and present infection. Antibodies were measured in the plasma of children that are the offspring in a population-based birth cohort, the Avon Longitudinal Study of Parents and Children (ALSPAC). Plasma was collected during clinics at age 5, 7, 11 and 15 years. The antigens examined include: fungal (Saccharomyces cerevisiae); protozoan (Toxoplasma gondii and surface antigen 1 of T. gondii); herpes viruses (cytomegalovirus, Epstein-Barr virus, herpes simplex virus type 1); common colds (influenza virus subtypes H1N1 and H3N2); other antigens (measles); animal (feline herpes virus, Theiler’s virus); bacteria (Helicobacter pylori); dietary antigens (bovine casein alpha protein, bovine casein beta protein). Alongside the depth of data available within the ALSPAC cohort, this longitudinal resource will enable the investigation of the association between infections and a wide variety of outcomes.

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“…In a healthy organism, glucagon secretion is suppressed by hyperglycemia, but in type 1 DM, an elevated glucagon concentration aggravates metabolic defects due to insulin deficiency. In response to insulin deficiency, uncontrolled lipolysis and elevated levels of free fatty acids occur in the plasma [4]. On the other hand, type 2 DM comprises a group of genetic diseases with similar symptoms and outcomes, but with different genetic backgrounds and pathophysiological processes.…”

Section: Introductionmentioning

confidence: 99%

Wound Healing Process, Diabetes and Implications of Dipeptidyl Peptidase IV (DPP IV/CD26)

Pučar¹,

Kovač²,

Detel³

et al. 2017

J Tissue Sci Eng

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Dipeptidyl Peptidase IV or molecule CD26 (DPP IV/CD26) is a multifunctional protein, identified as a therapeutic target for type 2 diabetes, due to its ability to degrade incretins, insulin secretagogues. Delayed wound healing is a significant complication in diabetic patients that represents a major socio-economic health problem. It has been proposed that DPP IV/CD26 inhibition accelerates healing of chronic diabetic ulcers in those patients, through the induction of a histological pattern consistent with enhanced angiogenesis. Studies on mice models of diabetesdisturbed wound healing also suggested that the inhibition of DPP IV enzymatic activity may improve tissue regeneration processes. However, further research is needed to elucidate the role of DPP IV/CD26 in diabetic wound healing. The objective of this work was to discuss recent findings on the implications of DPP IV/CD26 in tissue regeneration and reparation in diabetic environment.

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Type 1 diabetes: where are we in 2017?

Cited by 24 publications

References 43 publications

Impaired Gastric Hormone Regulation of Osteoblasts and Lysyl Oxidase Drives Bone Disease in Diabetes Mellitus

Impaired Gastric Hormone Regulation of Osteoblasts and Lysyl Oxidase Drives Bone Disease in Diabetes Mellitus

Longitudinal serological measures of common infection in the Avon Longitudinal Study of Parents and Children cohort

Wound Healing Process, Diabetes and Implications of Dipeptidyl Peptidase IV (DPP IV/CD26)

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