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Diabetes Complications: From Pathophysiology to Novel Therapeutic Approaches

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A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (31 December 2020) | Viewed by 50742

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Dr. Istvan Kovanecz

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Guest Editor

1. The Lundquist Institute, Torrance, CA, USA
2. David Geffen School of Medicine at UCLA, Los Angeles, CA, USA
Interests: diabetes-related complications; metabolic syndrome; sexual dysfunction; urinary incontinence; cardiac-, skeletal- and smooth muscle regeneration; stem cell and gene therapy

Special Issue Information

Dear Colleagues,

The Special Issue, “Diabetes Complications: From Pathophysiology to Novel Therapeutic Approaches”, will focus on the molecular pathophysiology of diabetes mellitus and its devastating complications, as well as new biomarkers for early detection, and novel therapeutic approaches.

Diabetes mellitus has become a worldwide epidemic in recent decades. A global survey estimated more than half a billion cases of T2DM in 2018, and the number is rapidly rising. Long-term complications of T2DM cause a wide range of increasingly prevalent debilitating co-morbidities with complex pathophysiology in diabetic patients. A more comprehensive understanding of the underlying molecular processes and identification of key molecules could lead to a more precisely targeted intervention either for prevention or for treatment. Monitoring changes in the global gene expression profile, refined by global micro RNA expression profiling, could provide the necessary clues to find those key components and biomarkers. This Special Issue is open for original articles and reviews in basic, clinical, and translational, as well as multidisciplinary research, including but not limited to the following diabetes-related topics:

Cardiovascular disease
Hyperlipidemia
Neuropathy
Erectile dysfunction
Nephropathy
Retinopathy
Skin conditions
Impaired wound healing
Hearing impairment
Psychological effects

Dr. Istvan Kovanecz
Guest Editor

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Keywords

diabetes complications
epigenetic imprinting
molecular profiling
biomarkers
targeted therapy
glucose control
conventional and complementary approaches
stem cell damage
vascular damage and regeneration

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Related Special Issue

Diabetes Complications: From Pathophysiology to Novel Therapeutic Approaches 2.0 in Biomedicines (3 articles)

Published Papers (11 papers)

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Research

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13 pages, 2557 KiB

Open AccessArticle

Role of Cutaneous Aquaporins in the Development of Xeroderma in Type 2 Diabetes

by Nobutomo Ikarashi, Nanaho Mizukami, Chenchen Pei, Ryogo Uchino, Izumi Fujisawa, Natsuko Fukuda, Risako Kon, Hiroyasu Sakai and Junzo Kamei

Biomedicines 2021, 9(2), 104; https://doi.org/10.3390/biomedicines9020104 - 21 Jan 2021

Cited by 12 | Viewed by 2490

Abstract

Xeroderma is induced by diabetes, reducing patients’ quality of life. We aimed to clarify the roles of cutaneous water channel aquaporin-3 (AQP3) in diabetic xeroderma using type 2 diabetes model db/db mice. Blood glucose levels were unchanged in 5-week-old db/db mice compared to db/+ mice (control mice), but the pathophysiology of type 2 diabetes was confirmed in 12-week-old db/db mice. The dermal water content and AQP3 expression in 5-week-old db/db mice were almost the same as those in the control mice. On the other hand, in 12-week-old db/db mice, the dermal water content and AQP3 expression were significantly decreased. The addition of glucose to HaCaT cells had no effect on AQP3, but tumor necrosis factor-α (TNF-α) decreased the AQP3 expression level. Blood TNF-α levels or skin inflammation markers in the 12-week-old db/db mice were significantly higher than those in control mice. AQP3 levels in the skin were decreased in type 2 diabetes, and this decrease in AQP3 may be one of the causes of xeroderma. Therefore, a substance that increases AQP3 may be useful for improving xeroderma. Additionally, a decrease in skin AQP3 may be triggered by inflammation. Therefore, anti-inflammatory drugs may be effective as new therapeutic agents for diabetic xerosis. Full article

(This article belongs to the Special Issue Diabetes Complications: From Pathophysiology to Novel Therapeutic Approaches)

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13 pages, 3432 KiB

Open AccessArticle

GADD45β Regulates Hepatic Gluconeogenesis via Modulating the Protein Stability of FoxO1

by Hyunmi Kim, Da Som Lee, Tae Hyeon An, Tae-Jun Park, Eun-Woo Lee, Baek Soo Han, Won Kon Kim, Chul-Ho Lee, Sang Chul Lee, Kyoung-Jin Oh and Kwang-Hee Bae

Biomedicines 2021, 9(1), 50; https://doi.org/10.3390/biomedicines9010050 - 8 Jan 2021

Cited by 6 | Viewed by 3618

Abstract

Increased hepatic gluconeogenesis is one of the main contributors to the development of type 2 diabetes. Recently, it has been reported that growth arrest and DNA damage-inducible 45 beta (GADD45β) is induced under both fasting and high-fat diet (HFD) conditions that stimulate hepatic gluconeogenesis. Here, this study aimed to establish the molecular mechanisms underlying the novel role of GADD45β in hepatic gluconeogenesis. Both whole-body knockout (KO) mice and adenovirus-mediated knockdown (KD) mice of GADD45β exhibited decreased hepatic gluconeogenic gene expression concomitant with reduced blood glucose levels under fasting and HFD conditions, but showed a more pronounced effect in GADD45β KD mice. Further, in primary hepatocytes, GADD45β KD reduced glucose output, whereas GADD45β overexpression increased it. Mechanistically, GADD45β did not affect Akt-mediated forkhead box protein O1 (FoxO1) phosphorylation and forskolin-induced cAMP response element-binding protein (CREB) phosphorylation. Rather it increased FoxO1 transcriptional activity via enhanced protein stability of FoxO1. Further, GADD45β colocalized and physically interacted with FoxO1. Additionally, GADD45β deficiency potentiated insulin-mediated suppression of hepatic gluconeogenic genes, and it were impeded by the restoration of GADD45β expression. Our finding demonstrates GADD45β as a novel and essential regulator of hepatic gluconeogenesis. It will provide a deeper understanding of the FoxO1-mediated gluconeogenesis. Full article

(This article belongs to the Special Issue Diabetes Complications: From Pathophysiology to Novel Therapeutic Approaches)

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11 pages, 4884 KiB

Open AccessArticle

The Acceleration of Diabetic Wound Healing by Low-Intensity Extracorporeal Shockwave Involves in the GSK-3β Pathway

by Rong-Fu Chen, Yun-Nan Lin, Keng-Fan Liu, Chun-Ting Wang, Savitha Ramachandran, Ching-Jen Wang and Yur-Ren Kuo

Biomedicines 2021, 9(1), 21; https://doi.org/10.3390/biomedicines9010021 - 30 Dec 2020

Cited by 9 | Viewed by 3315

Abstract

Previous studies have demonstrated that extracorporeal shock wave therapy (ESWT) could accelerate diabetic wound healing and that the inhibition of glycogen synthase kinase-3β (GSK-3β) is involved in epithelial differentiation during wound healing. This study investigated whether the enhancement of diabetic wound healing by ESWT is associated with the GSK-3β-mediated Wnt/β-catenin signaling pathway. A dorsal skin wounding defect model using streptozotocin-induced diabetic rodents was established. Rats were divided into 4 groups: group 1, normal controls without diabetes; group 2, diabetic controls without treatment; group 3, diabetic rats receiving ESWT; and group 4, rats receiving 6-bromoindirubin-3′oxime (BIO), a GSK-3β inhibitor, to trigger Wnt/β-catenin signaling. Tissue samples were collected and analyzed by immunohistochemical (IHC) staining and quantitative RT-PCR. The ESWT and BIO-treated groups both exhibited significant promotion of wound healing compared to the healing in controls without treatment. RT-PCR analysis of Wnt-1, -3a, -4, -5a, and -10 and β-catenin expression showed significantly increased expression in the ESWT group. The IHC staining showed that Wnt-3a and -5a and β-catenin levels were significantly increased in the ESWT and BIO treatment groups compared to the control groups. ESWT enhancement of diabetic wound healing is associated with modulation of the GSK-3β-mediated Wnt/β-catenin signaling pathway. Full article

(This article belongs to the Special Issue Diabetes Complications: From Pathophysiology to Novel Therapeutic Approaches)

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19 pages, 13247 KiB

Open AccessArticle

Adenosine A_2A and A₃ Receptors as Targets for the Treatment of Hypertensive-Diabetic Nephropathy

by Daniela Patinha, Carla Abreu, Carla Carvalho, Olga Mariana Cunha, Mariana Mota, Joana Afonso, Teresa Sousa, António Albino-Teixeira, Carmen Diniz and Manuela Morato

Biomedicines 2020, 8(11), 529; https://doi.org/10.3390/biomedicines8110529 - 23 Nov 2020

Cited by 11 | Viewed by 4490

Abstract

Diabetic nephropathy (DN) and hypertension are prime causes for end-stage renal disease (ESRD) that often coexist in patients, but are seldom studied in combination. Kidney adenosine levels are markedly increased in diabetes, and the expression and function of renal adenosine receptors are altered in experimental diabetes. The aim of this work is to explore the impact of endogenous and exogenous adenosine on the expression/distribution profile of its receptors along the nephron of hypertensive rats with experimentally-induced diabetes. Using spontaneously hypertensive (SHR) rats rendered diabetic with streptozotocin (STZ), we show that treatment of SHR-STZ rats with an agonist of adenosine receptors increases A_2A immunoreactivity in superficial glomeruli (SG), proximal tubule (PCT), and distal tubule (DCT). Differently, treatment of SHR-STZ rats with a xanthinic antagonist of adenosine receptors decreases adenosine A₃ immunoreactivity in SG, PCT, DCT, and collecting duct. There is no difference in the immunoreactivity against the adenosine A₁ and A_2B receptors between the experimental groups. The agonist of adenosine receptors ameliorates renal fibrosis, probably via A_2A receptors, while the antagonist exacerbates it, most likely due to tonic activation of A₃ receptors. The reduction in adenosine A₃ immunoreactivity might be due to receptor downregulation in response to prolonged activation. Altogether, these results suggest an opposite regulation exerted by endogenous and exogenous adenosine upon the expression of its A_2A and A₃ receptors along the nephron of hypertensive diabetic rats, which has a functional impact and should be taken into account when considering novel therapeutic targets for hypertensive-diabetic nephropathy. Full article

(This article belongs to the Special Issue Diabetes Complications: From Pathophysiology to Novel Therapeutic Approaches)

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10 pages, 2486 KiB

Open AccessArticle

SGLT2 Inhibitor-Induced Sympathoexcitation in White Adipose Tissue: A Novel Mechanism for Beiging

by Jennifer R. Matthews, Lakshini Y. Herat, Aaron L. Magno, Shelley Gorman, Markus P. Schlaich and Vance B. Matthews

Biomedicines 2020, 8(11), 514; https://doi.org/10.3390/biomedicines8110514 - 18 Nov 2020

Cited by 12 | Viewed by 2985

Abstract

Recent preclinical data show that sodium glucose cotransporter 2 (SGLT2) inhibitors are able to reduce weight gain and induce beiging in white adipose tissue (WAT). We have previously shown that in neurogenic hypertensive Schlager (BPH/2J) mice, treatment with the SGLT2 inhibitor, Dapagliflozin, reduced blood pressure and prevented weight gain. Here we show that chemical sympathetic denervation achieved by systemic administration of 6-hydroxy-dopamine (6-OHDA) reduces body weight and the heightened sympathetic nervous system (SNS) innervation in WAT. Furthermore, we demonstrate that 2 weeks of Dapagliflozin treatment increases SNS innervation in WAT of hypertensive mice. This increase is accompanied by a non-significant elevation in mRNA levels of the Ucp1 and Pgc-1α genes, which are markers of beiging. No significant difference in the mRNA levels of the inflammatory mediators Il-6 and Tnf-α were detected in WAT of Dapagliflozin treated mice. These findings suggest that SGLT-2 inhibitor-associated prevention of weight gain may be mediated, at least in part, by inducing the beiging of WAT. Full article

(This article belongs to the Special Issue Diabetes Complications: From Pathophysiology to Novel Therapeutic Approaches)

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15 pages, 1858 KiB

Open AccessArticle

Effect of Ezetimibe on Glucose Metabolism and Inflammatory Markers in Adipose Tissue

by Yongin Cho, Ryeong-Hyeon Kim, Hyunki Park, Hye Jin Wang, Hyangkyu Lee and Eun Seok Kang

Biomedicines 2020, 8(11), 512; https://doi.org/10.3390/biomedicines8110512 - 18 Nov 2020

Cited by 17 | Viewed by 4999

Abstract

Despite numerous studies, the effects of ezetimibe on glucose metabolism are poorly understood. Here, we aimed to investigate the effects of ezetimibe on glucose metabolism and the expression of inflammatory markers. Thirteen rats were randomly assigned to an ezetimibe (n = 6) or control group (n = 7). The control group received a high fat diet (HFD; 60 Kcal%), whereas the ezetimibe group received an HFD (60 Kcal%) containing 160 mg/kg of ezetimibe. After 14 weeks, adipose and liver tissues, along with plasma, were collected and comparatively analyzed. The effects of combination therapy with ezetimibe and statins on glucose metabolism were investigated over a 1-year period using data from patients with hyperlipidemia. Several indices of glucose metabolism partially improved in the ezetimibe group. The sizes of adipocytes and the accumulation of pro-inflammatory cytokines were reduced in the ezetimibe group. Ezetimibe treatment induced anti-inflammatory cytokines and fatty acid oxidation in adipocytes and reduced serum levels of free fatty acids. Clinical data analysis revealed that statin monotherapy significantly increased insulin resistance. However, combination therapy with ezetimibe and statins did not increase insulin resistance. In conclusion, ezetimibe was found to reduce the sizes of adipocytes in visceral fat and serum levels of free fatty acids, to induce fatty acid oxidation, to improve adipocytic inflammation, and to partially improve glycemic index values. Full article

(This article belongs to the Special Issue Diabetes Complications: From Pathophysiology to Novel Therapeutic Approaches)

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15 pages, 1645 KiB

Open AccessArticle

Evidence of Altered Peripheral Nerve Function in a Rodent Model of Diet-Induced Prediabetes

by Md Jakir Hossain, Michael D. Kendig, Brandon M. Wild, Tushar Issar, Arun V. Krishnan, Margaret J. Morris and Ria Arnold

Biomedicines 2020, 8(9), 313; https://doi.org/10.3390/biomedicines8090313 - 28 Aug 2020

Cited by 12 | Viewed by 4563

Abstract

Peripheral neuropathy (PN) is a debilitating complication of diabetes that affects >50% of patients. Recent evidence suggests that obesity and metabolic disease, which often precede diabetes diagnosis, may influence PN onset and severity. We examined this in a translationally relevant model of prediabetes induced by a cafeteria (CAF) diet in Sprague–Dawley rats (n = 15 CAF versus n = 15 control). Neuropathy phenotyping included nerve conduction, tactile sensitivity, intraepidermal nerve fiber density (IENFD) and nerve excitability testing, an in vivo measure of ion channel function and membrane potential. Metabolic phenotyping included body composition, blood glucose and lipids, plasma hormones and inflammatory cytokines. After 13 weeks diet, CAF-fed rats demonstrated prediabetes with significantly elevated fasting blood glucose, insulin and impaired glucose tolerance as well as obesity and dyslipidemia. Nerve conduction, tactile sensitivity and IENFD did not differ; however, superexcitability was significantly increased in CAF-fed rats. Mathematical modeling demonstrated this was consistent with a reduction in sodium–potassium pump current. Moreover, superexcitability correlated positively with insulin resistance and adiposity, and negatively with fasting high-density lipoprotein cholesterol. In conclusion, prediabetic rats over-consuming processed, palatable foods demonstrated altered nerve function that preceded overt PN. This work provides a relevant model for pathophysiological investigation of diabetic complications. Full article

(This article belongs to the Special Issue Diabetes Complications: From Pathophysiology to Novel Therapeutic Approaches)

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25 pages, 2899 KiB

Open AccessReview

β-Cell Dysfunction, Hepatic Lipid Metabolism, and Cardiovascular Health in Type 2 Diabetes: New Directions of Research and Novel Therapeutic Strategies

by Ahmad Al-Mrabeh

Biomedicines 2021, 9(2), 226; https://doi.org/10.3390/biomedicines9020226 - 23 Feb 2021

Cited by 17 | Viewed by 4026

Abstract

Cardiovascular disease (CVD) remains a major problem for people with type 2 diabetes mellitus (T2DM), and dyslipidemia is one of the main drivers for both metabolic diseases. In this review, the major pathophysiological and molecular mechanisms of β-cell dysfunction and recovery in T2DM are discussed in the context of abnormal hepatic lipid metabolism and cardiovascular health. (i) In normal health, continuous exposure of the pancreas to nutrient stimulus increases the demand on β-cells. In the long term, this will not only stress β-cells and decrease their insulin secretory capacity, but also will blunt the cellular response to insulin. (ii) At the pre-diabetes stage, β-cells compensate for insulin resistance through hypersecretion of insulin. This increases the metabolic burden on the stressed β-cells and changes hepatic lipoprotein metabolism and adipose tissue function. (iii) If this lipotoxic hyperinsulinemic environment is not removed, β-cells start to lose function, and CVD risk rises due to lower lipoprotein clearance. (iv) Once developed, T2DM can be reversed by weight loss, a process described recently as remission. However, the precise mechanism(s) by which calorie restriction causes normalization of lipoprotein metabolism and restores β-cell function are not fully established. Understanding the pathophysiological and molecular basis of β-cell failure and recovery during remission is critical to reduce β-cell burden and loss of function. The aim of this review is to highlight the link between lipoprotein export and lipid-driven β-cell dysfunction in T2DM and how this is related to cardiovascular health. A second aim is to understand the mechanisms of β-cell recovery after weight loss, and to explore new areas of research for developing more targeted future therapies to prevent T2DM and the associated CVD events. Full article

(This article belongs to the Special Issue Diabetes Complications: From Pathophysiology to Novel Therapeutic Approaches)

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19 pages, 501 KiB

Open AccessReview

Metabolic Diseases and Down Syndrome: How Are They Linked Together?

by Manon Moreau, Soukaina Benhaddou, Rodolphe Dard, Stefania Tolu, Rim Hamzé, François Vialard, Jamileh Movassat and Nathalie Janel

Biomedicines 2021, 9(2), 221; https://doi.org/10.3390/biomedicines9020221 - 22 Feb 2021

Cited by 32 | Viewed by 6822

Abstract

Down syndrome is a genetic disorder caused by the presence of a third copy of chromosome 21, associated with intellectual disabilities. Down syndrome is associated with anomalies of both the nervous and endocrine systems. Over the past decades, dramatic advances in Down syndrome research and treatment have helped to extend the life expectancy of these patients. Improved life expectancy is obviously a positive outcome, but it is accompanied with the need to address previously overlooked complications and comorbidities of Down syndrome, including obesity and diabetes, in order to improve the quality of life of Down syndrome patients. In this focused review, we describe the associations between Down syndrome and comorbidities, obesity and diabetes, and we discuss the understanding of proposed mechanisms for the association of Down syndrome with metabolic disorders. Drawing molecular mechanisms through which Type 1 diabetes and Type 2 diabetes could be linked to Down syndrome could allow identification of novel drug targets and provide therapeutic solutions to limit the development of metabolic and cognitive disorders. Full article

(This article belongs to the Special Issue Diabetes Complications: From Pathophysiology to Novel Therapeutic Approaches)

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17 pages, 1444 KiB

Open AccessReview

PPARα Agonist Oral Therapy in Diabetic Retinopathy

by Yohei Tomita, Deokho Lee, Kazuo Tsubota and Toshihide Kurihara

Biomedicines 2020, 8(10), 433; https://doi.org/10.3390/biomedicines8100433 - 19 Oct 2020

Cited by 29 | Viewed by 4603

Abstract

Diabetic retinopathy (DR) is an eye condition that develops after chronically poorly-managed diabetes, and is presently the main cause for blindness on a global scale. Current treatments for DR such as laser photocoagulation, topical injection of corticosteroids, intravitreal injection of anti-vascular endothelial growth factor (VEGF) agents and vitreoretinal surgery are only applicable at the late stages of DR and there are possibilities of significant adverse effects. Moreover, the forms of treatment available for DR are highly invasive to the eyes. Safer and more effective pharmacological treatments are required for DR treatment, in particular at an early stage. In this review, we cover recently investigated promising oral pharmacotherapies, the methods of which are safer, easier to use, patient-friendly and pain-free, in clinical studies. We especially focus on peroxisome proliferator-activator receptor alpha (PPARα) agonists in which experimental evidence suggests PPARα activation may be closely related to the attenuation of vascular damages, including lipid-induced toxicity, inflammation, an excess of free radical generation, endothelial dysfunction and angiogenesis. Furthermore, oral administration of selective peroxisome proliferator-activated receptor alpha modulator (SPPARMα) agonists may induce hepatic fibroblast growth factor 21 expression, indirectly resulting in retinal protection in animal studies. Our review will enable more comprehensive approaches for understanding protective roles of PPARα for the prevention of DR development. Full article

(This article belongs to the Special Issue Diabetes Complications: From Pathophysiology to Novel Therapeutic Approaches)

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45 pages, 3809 KiB

Open AccessEditor’s ChoiceReview

Free Fatty Acid Receptors 2 and 3 as Microbial Metabolite Sensors to Shape Host Health: Pharmacophysiological View

by Sidharth P. Mishra, Prashantha Karunakar, Subhash Taraphder and Hariom Yadav

Biomedicines 2020, 8(6), 154; https://doi.org/10.3390/biomedicines8060154 - 8 Jun 2020

Cited by 65 | Viewed by 7658

Abstract

The role of the gut microbiome in human health is becoming apparent. The major functional impact of the gut microbiome is transmitted through the microbial metabolites that are produced in the gut and interact with host cells either in the local gut environment or are absorbed into circulation to impact distant cells/organs. Short-chain fatty acids (SCFAs) are the major microbial metabolites that are produced in the gut through the fermentation of non-digestible fibers. SCFAs are known to function through various mechanisms, however, their signaling through free fatty acid receptors 2 and 3 (FFAR2/3; type of G-coupled protein receptors) is a new therapeutic approach. FFAR2/3 are widely expressed in diverse cell types in human and mice, and function as sensors of SCFAs to change several physiological and cellular functions. FFAR2/3 modulate neurological signaling, energy metabolism, intestinal cellular homeostasis, immune response, and hormone synthesis. FFAR2/3 function through Gi and/or Gq signaling, that is mediated through specific structural features of SCFAs-FFAR2/3 bindings and modulating specific signaling pathway. In this review, we discuss the wide-spread expression and structural homologies between human and mice FFAR2/3, and their role in different human health conditions. This information can unlock opportunities to weigh the potential of FFAR2/3 as a drug target to prevent human diseases. Full article

(This article belongs to the Special Issue Diabetes Complications: From Pathophysiology to Novel Therapeutic Approaches)

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