Decreased basal and stimulated salivary parameters by histopathological lesions and secretory dysfunction of parotid and submandibular glands in rats with type�2 diabetes

Chen, Siyu; Wang, Ying; Zhang, Chunlei; Yang, Ze-Min

doi:10.3892/etm.2020.8505

Cited by 17 publications

(13 citation statements)

References 23 publications

(28 reference statements)

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“…We showed that STZ injection promoted degenerative changes in the form of vacuolations in both acinar and ductal cells of parotid gland. These results were consistent with previous studies demonstrating that diabetes likely induces morphological alterations in salivary glands that are of a lipid nature as they are removed during the fixation and processing of the samples [ 10 , 11 , 13 , 16 – 18 ]. In diabetes, vacuolations are more evident in the parotid gland than in the submandibular glands [ 10 , 17 ].…”

Section: Discussionsupporting

confidence: 93%

“…The majority of oral changes related to salivary gland dysfunction are characterised by hyposalivation and xerostomia, which significantly reduce the quality of life in patients with diabetes [ 5 – 7 ]. Both basal and stimulated secretion of the parotid and submandibular glands are dramatically downregulated under prolonged hyperglycaemia in humans and rats [ 8 – 11 ].…”

Section: Introductionmentioning

confidence: 99%

“…These salivary gland changes are likely caused by diabetes-induced oxidative damage. Several studies have reported that the parotid glands are more vulnerable to both antioxidant disturbances and oxidative damage, demonstrating prominent degenerative changes [ 10 , 11 , 17 , 19 , 20 ]. Indeed, upon stimulation, the parotid gland, one of the main salivary glands, secretes more than 50% of the total saliva [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

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Human dental pulp stem cells attenuate streptozotocin-induced parotid gland injury in rats

2021

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Objective Diabetes mellitus causes deterioration in the body, including serious damage of the oral cavity related to salivary gland dysfunction, characterised by hyposalivation and xerostomia. Human dental pulp stem cells (hDPSCs) represent a promising therapy source, due to the easy, minimally invasive surgical access to these cells and their high proliferative capacity. It was previously reported that the trophic support mediated by these cells can rescue the functional and structural alterations of damaged salivary glands. However, potential differentiation and paracrine effects of hDPSCs in diabetic-induced parotid gland damage have not been investigated. Our study aimed to investigate the therapeutic effects of intravenous transplantation of hDPSCs on parotid gland injury in a rat model of streptozotocin (STZ)-induced type 1 diabetes. Methods Thirty Sprague–Dawley male rats were randomly categorised into three groups: control, diabetic (STZ), and transplanted (STZ + hDPSCs). The hDPSCs or the vehicles were injected into the rats’ tail veins, 7 days after STZ injection. Fasting blood glucose levels were monitored weekly. A glucose tolerance test was performed, and the parotid gland weight, salivary flow rate, oxidative stress indices, parotid gland histology, and caspase-3, vascular endothelial growth factor, proliferating cell nuclear antigen, neuronal nitric oxide synthase, endothelial nitric oxide synthase, and tetrahydrobiopterin biosynthetic enzyme expression levels in parotid tissues were assessed 28 days post-transplantation. Results Transplantation of hDPSCs decreased blood glucose, improved parotid gland weight and salivary flow rate, and reduced oxidative stress. The cells migrated to the STZ-injured parotid gland and differentiated into acinar, ductal, and myoepithelial cells. Moreover, hDPSCs downregulated the expression of caspase-3 and upregulated the expression of vascular endothelial growth factor and proliferating cell nuclear antigen, likely exerting pro-angiogenic and anti-apoptotic effects and promoting endogenous regeneration. In addition, the transplanted cells enhanced the parotid nitric oxide-tetrahydrobiopterin pathway. Conclusions Our results showed that hDPSCs migrated to and survived within the STZ-injured parotid gland, where functional and morphological damage was prevented due to the restoration of normal glucose levels, differentiation into parotid cell populations, and stimulation of paracrine-mediated regeneration. Thus, hDPSCs may have potential in the treatment of diabetes-induced parotid gland injury.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Human dental pulp stem cells attenuate streptozotocin-induced parotid gland injury in rats

2021

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“…It is noteworthy that maternal type 1 diabetes induced postnatal changes in the development of rat SG in offspring, including decreased AQP5 expression [ 126 ]. Rats with type 2 diabetes displayed decreased saliva flow, inflammatory cell infiltration of SG and decreased AQP5 expression [ 127 ]. Further studies are required to fully assess the role of AQP5 in diabetic xerostomia.…”

Section: Involvement Of Aqps In Sg Pathologiesmentioning

confidence: 99%

Insight into Salivary Gland Aquaporins

D’Agostino

Elkashty

Chivasso

et al. 2020

Cells

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The main role of salivary glands (SG) is the production and secretion of saliva, in which aquaporins (AQPs) play a key role by ensuring water flow. The AQPs are transmembrane channel proteins permeable to water to allow water transport across cell membranes according to osmotic gradient. This review gives an insight into SG AQPs. Indeed, it gives a summary of the expression and localization of AQPs in adult human, rat and mouse SG, as well as of their physiological role in SG function. Furthermore, the review provides a comprehensive view of the involvement of AQPs in pathological conditions affecting SG, including Sjögren’s syndrome, diabetes, agedness, head and neck cancer radiotherapy and SG cancer. These conditions are characterized by salivary hypofunction resulting in xerostomia. A specific focus is given on current and future therapeutic strategies aiming at AQPs to treat xerostomia. A deeper understanding of the AQPs involvement in molecular mechanisms of saliva secretion and diseases offered new avenues for therapeutic approaches, including drugs, gene therapy and tissue engineering. As such, AQP5 represents a potential therapeutic target in different strategies for the treatment of xerostomia.

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“…AQP5 is also downregulated in the parotid salivary gland of T2D rats that showed decreased salivary flow rate [ 138 ]. Rats treatment with bone marrow-derived stem cells improves the salivary flow rate and alters AQP5 levels in the parotid gland [ 139 ].…”

Section: Possible Role Of Aqps “Metabolic Network” In Obesity-induced Systemic Insulin Resistancementioning

confidence: 99%

Aquaporins in insulin resistance and diabetes: More than channels!

et al. 2021

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Aquaporins (AQPs) are part of the family of the integral membrane proteins. Their function is dedicated to the transport of water, glycerol, ammonia, urea, H 2 O 2 , and other small molecules across the biological membranes. Although for many years they were scarcely considered, AQPs have a relevant role in the development of many diseases. Recent discoveries suggest, that AQPs may play an important role in the process of fat accumulation and regulation of oxidative stress, two crucial aspects of insulin resistance and type-2 diabetes (T2D). Insulin resistance (IR) and T2D are multi-faceted systemic diseases with multiple connections to obesity and other comorbidities such as hypertension, dyslipidemia and metabolic syndrome. Both IR and T2D transcends different tissues and organs, creating the maze of mutual relationships between adipose fat depots, skeletal muscle, liver and other insulin-sensitive organs. AQPs with their heterogenous properties, distinctive tissue distribution and documented involvement in both the lipid metabolism and regulation of the oxidative stress appear to be feasible candidates in the search for the explanation to this third-millennium plague. A lot of research has been assigned to adipose tissue AQP7 and liver tissue AQP9, clarifying their relationship and coordinated work in the induction of hepatic insulin resistance. Novel research points also to other aquaporins, such as AQP11 which may be associated with the induction of insulin resistance and T2D through its involvement in hydrogen peroxide transport. In this review we collected recent discoveries in the field of AQP's involvement in the insulin resistance and T2D. Novel paths which connect AQPs with metabolic disorders can give new fuel to the research on obesity, insulin resistance and T2D - one of the most worrying problems of the modern society.

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Decreased basal and stimulated salivary parameters by histopathological lesions and secretory dysfunction of parotid and submandibular glands in rats with type�2 diabetes

Cited by 17 publications

References 23 publications

Human dental pulp stem cells attenuate streptozotocin-induced parotid gland injury in rats

Human dental pulp stem cells attenuate streptozotocin-induced parotid gland injury in rats

Insight into Salivary Gland Aquaporins

Aquaporins in insulin resistance and diabetes: More than channels!

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