Streptozocin-induced type-1 diabetes mellitus results in decreased density of CGRP sensory and TH sympathetic nerve fibers that are positively correlated with bone loss at the mouse femoral neck

Enríquez-Pérez, Iris A.; Galindo-Ordoñez, Karla E.; Pantoja-Ortíz, Christian E.; A, Martínez-Martínez; Acosta-González, Rosa Issel; Muñoz-Islas, Enriqueta; Jiménez-Andrade, Juan Miguel

doi:10.1016/j.neulet.2017.06.042

Cited by 25 publications

(15 citation statements)

References 28 publications

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“…It is possible that the effects of C-peptide may also be exerted via blood glucose control, or by improving the response to insulin action. In fact, in line with previous reports of an increased whole body glucose utilization [43,44] and glucose transport in skeletal muscle [45], in our study, C-peptide treatment prevented the hyperglycaemia seen in D-CTR (Table 1, Supplementary Fig. 2).…”

Section: Discussionsupporting

confidence: 93%

Effects of C-Peptide Replacement Therapy on Bone Microarchitecture Parameters in Streptozotocin-Diabetic Rats

et al. 2020

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C-peptide therapy protects against diabetic micro-and macrovascular damages and neuropatic complications. However, to date, the role of C-peptide in preventing diabetes-related bone loss has not been investigated. Our aim was to evaluate if C-peptide infusion improves bone quality in diabetic rats. Twenty-three male Wistar rats were randomly divided into three groups: normal control group; sham diabetic control group; diabetic plus C-peptide group. Diabetes was induced by streptozotocin injection and C-peptide was delivered subcutaneously for 6 weeks. We performed micro-CT and histological testing to assess several trabecular microarchitectural parameters. At the end, diabetic plus C-peptide rats had a higher serum C-peptide (p = 0.02) and calcium (p = 0.04) levels and tibia weight (p = 0.02) than the diabetic control group. The diabetic plus C-peptide group showed a higher trabecular thickness and cross-sectional thickness than the diabetic control group (p = 0.01 and p = 0.03). Both the normal control and diabetic plus C-peptide groups had more Runx-2 and PLIN1 positive cells in comparison with the diabetic control group (p = 0.045 and p = 0.034). Diabetic rats receiving C-peptide had higher quality of trabecular bone than diabetic rats not receiving this treatment. If confirmed, C-peptide could have a role in improving bone quality in diabetes. Keywords c-peptide • Bone microarchitectural parameters • Type 1 diabetes mellitus • Osteoporosis • Diabetic rat model Electronic supplementary material The online version of this article (

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Section: Discussionsupporting

confidence: 93%

Effects of C-Peptide Replacement Therapy on Bone Microarchitecture Parameters in Streptozotocin-Diabetic Rats

et al. 2020

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“…In diabetic individuals, CGRP and substance P levels are decreased ( 21 , 22 , 24 ). Moreover, it has been reported that in an experimental model of type 1 diabetes there is a decrease in or an impairment of CGRPergic sensory nerves ( 181 , 182 ). In addition, it is well-known that CGRP is a potent vasodilator which is associated with glucose metabolism.…”

Section: Association Between Migraine and Diabetes Mellitus (Dm)mentioning

confidence: 99%

Metabolic Aspects of Migraine: Association With Obesity and Diabetes Mellitus

et al. 2021

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Migraine is a disabling neurovascular disorder, characterized by moderate to severe unilateral headaches, nausea, photophobia, and/or phonophobia, with a higher prevalence in women than in men, which can drastically affect the quality of life of migraine patients. In addition, this chronic disorder is related with metabolic comorbidities associated with the patient's lifestyle, including obesity and diabetes mellitus (DM). Beyond the personal and socioeconomic impact caused by migraine, obesity and DM, it has been suggested that these metabolic disorders seem to be related to migraine since: (i) they are a risk factor for developing cardiovascular disorders or chronic diseases; (ii) they can be influenced by genetic and environmental risk factors; and (iii) while clinical and epidemiological studies suggest that obesity is a risk factor for migraine, DM (i.e., type 1 and type 2 DM) have been reported to be either a protective or a risk factor in migraine. On this basis, and given the high worldwide prevalence of migraine, obesity, and DM, this article provides a narrative review of the current literature related to the association between the etiology and pathophysiology of migraine and these metabolic disorders, considering lifestyle aspects, as well as the possible involvement of neurotransmitters, neuropeptides, and/or sex hormones. While a link between migraine and metabolic disorders has been suggested, many studies are contradictory and the mechanisms involved in this association are not yet sufficiently established. Therefore, further research should be focused on understanding the possible mechanisms involved.

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“…According to the present results, this was mainly a cause of reduced osteoblastogenesis. Accordingly, Enriquez et al induced type 1 diabetes in rodents by streptozocin injection and could proof a decreased bone trabecular thickness associated with decreased tyrosinhydroxylase positive sympathetic nerve fibers [ 34 ]. Very recently, Bubb et al were able to show that beta 3-agonist treatment markedly increases angiogenesis in a murine diabetic model of peripheral arterial disease [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

Role of Autonomous Neuropathy in Diabetic Bone Regeneration

Wagner

Wallner

Becerikli

et al. 2022

Cells

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Diabetes mellitus has multiple negative effects on regenerative processes, especially on wound and fracture healing. Despite the well-known negative effects of diabetes on the autonomous nervous system, only little is known about the role in bone regeneration within this context. Subsequently, we investigated diabetic bone regeneration in db−/db− mice with a special emphasis on the sympathetic nervous system of the bone in a monocortical tibia defect model. Moreover, the effect of pharmacological sympathectomy via administration of 6-OHDA was evaluated in C57Bl6 wildtype mice. Diabetic animals as well as wildtype mice received a treatment of BRL37344, a β3-adrenergic agonist. Bones of animals were examined via µCT, aniline-blue and Masson–Goldner staining for new bone formation, TRAP staining for bone turnover and immunoflourescence staining against tyrosinhydroxylase and stromal cell-derived factor 1 (SDF-1). Sympathectomized wildtype mice showed a significantly decreased bone regeneration, just comparable to db−/db− mice. New bone formation of BRL37344 treated db−/db− and sympathectomized wildtype mice was markedly improved in histology and µCT. Immunoflourescence stainings revealed significantly increased SDF-1 due to BRL37344 treatment in diabetic animals and sympathectomized wildtypes. This study depicts the important role of the sympathetic nervous system for bone regenerative processes using the clinical example of diabetes mellitus type 2. In order to improve and gain further insights into diabetic fracture healing, β3-agonist BRL37344 proved to be a potent treatment option, restoring impaired diabetic bone regeneration.

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Streptozocin-induced type-1 diabetes mellitus results in decreased density of CGRP sensory and TH sympathetic nerve fibers that are positively correlated with bone loss at the mouse femoral neck

Cited by 25 publications

References 28 publications

Effects of C-Peptide Replacement Therapy on Bone Microarchitecture Parameters in Streptozotocin-Diabetic Rats

Effects of C-Peptide Replacement Therapy on Bone Microarchitecture Parameters in Streptozotocin-Diabetic Rats

Metabolic Aspects of Migraine: Association With Obesity and Diabetes Mellitus

Role of Autonomous Neuropathy in Diabetic Bone Regeneration

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