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Special Issue "Metabolic Syndrome: From Molecular Mechanisms to Novel Therapies 2.0"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 11627

Special Issue Editors

Department of Internal Medicine and Medical Specialties (DIMIS), Università degli Studi di Palermo UNIPA, Palermo, Italy
Interests: cardiovascular risk; lipids; diabetes; prevention; therapy; Metabolic Syndrome; metabolism; lipoproteins; incretins; nutraceuticals
Special Issues, Collections and Topics in MDPI journals
Diabetes, Nutrition and Metabolic Diseases Department, Carol Davila University of Medicine and Pharmacy, 8 Eroii Sanitari Str., 050474 Bucharest, Romania
Interests: diabetes; nutrition; metabolic diseases; chronic kidney disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The metabolic syndrome (MetS) consists of a cluster of metabolic abnormalities including central obesity, insulin resistance, glucose intolerance, hypertension, and atherogenic dyslipidemia. It is rapidly emerging as a global health problem that increases the risk of developing type 2 diabetes and cardiovascular diseases. Early recognition using clinical parameters and inflammatory markers is imperative in order to reduce morbidity and possibly mortality, too, attributable to the syndrome. A number of susceptibility genes have been identified that are thought to play a role in the genetic etiology of MetS, thus paving the way to new molecular insights. Knowledge of the etiopathogenic pathways could facilitate novel therapeutic approaches to treating MetS. The link between MetS and diabetes and its complications, cardiovascular disease, and nephropathy is a newly developing paradigm with the central point being early atherosclerosis and endovascular inflammation. This Special Issue aims to provide an update on the latest research in MetS, shedding light on emerging markers unravelling molecular mechanisms and innovative remedies to be utilized in concert with lifestyle modifications.

Prof. Dr. Manfredi Rizzo
Prof. Dr. Anca Pantea Stoian
Prof. Dr. Ali Abbas Rizvi
Guest Editors

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • metabolic syndrome
  • risk factors
  • diabetes
  • cardiovascular disease
  • atherosclerosis
  • dyslipidemia
  • hypertension
  • obesity
  • insulin resistance
  • renal kidney disease
  • inflammation markers
  • molecular mechanism
  • oxidative stress
  • therapy
  • lifestyle

Published Papers (5 papers)

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Editorial

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Editorial
Metabolic Syndrome: From Molecular Mechanisms to Novel Therapies
Int. J. Mol. Sci. 2021, 22(18), 10038; https://doi.org/10.3390/ijms221810038 - 17 Sep 2021
Cited by 8 | Viewed by 1560
Abstract
The metabolic syndrome (MetS) consists of a cluster of metabolic abnormalities including central obesity, insulin resistance, glucose intolerance, hypertension, and atherogenic dyslipidemia [...] Full article
(This article belongs to the Special Issue Metabolic Syndrome: From Molecular Mechanisms to Novel Therapies 2.0)

Research

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Article
AICAR Improves Outcomes of Metabolic Syndrome and Type 2 Diabetes Induced by High-Fat Diet in C57Bl/6 Male Mice
Int. J. Mol. Sci. 2022, 23(24), 15719; https://doi.org/10.3390/ijms232415719 - 11 Dec 2022
Viewed by 556
Abstract
The aim of the study was to investigate the effect of AMP-activated protein kinase activator 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) on the consequences of metabolic syndrome and type 2 diabetes induced by the consumption of a high-fat diet (HFD) in male C57Bl/6 mice. Additionally, the [...] Read more.
The aim of the study was to investigate the effect of AMP-activated protein kinase activator 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) on the consequences of metabolic syndrome and type 2 diabetes induced by the consumption of a high-fat diet (HFD) in male C57Bl/6 mice. Additionally, the animals from group 6 were administered Methotrexate (MTX) at a dose of 1 mg/kg in parallel with AICAR, which slows down the metabolism of AICAR. The animals were recorded with signs of metabolic syndrome and type 2 diabetes mellitus by recording their body weights, glucose and insulin levels, and the calculating HOMA-IRs. At the end of the study, at the end of the 13th week, during necropsy, the internal organs were assessed, the masses of the organs were recorded, and special attention was paid to visceral fat, assessing its amount and the mass of the fat surrounding epididymis. The biochemical parameters and histology of the internal organs and tissues were assessed. The animals showed signs of metabolic syndrome and type 2 diabetes, namely, weight gain, hyperglycemia, hyperinsulinemia, an increase in the amount and mass of abdominal fat, and metabolic disorders, all expressed in a pathological change in biochemical parameters and pathological changes in internal organs. The AICAR treatment led to a decrease in body weight, a decrease in the amount and mass of abdominal fat, and an improvement in the pathomorphological picture of internal organs. However, some hepatotoxic effects were observed when the animals, on a received standard diet (STD), were treated with AICAR starting from the first day of the study. The additional administration of MTX, an AICAR metabolic inhibitor, did not improve its efficacy. Thus, AICAR has therapeutic potential for the treatment of metabolic syndrome and type 2 diabetes. Full article
(This article belongs to the Special Issue Metabolic Syndrome: From Molecular Mechanisms to Novel Therapies 2.0)
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Article
NAD+ Precursors Repair Mitochondrial Function in Diabetes and Prevent Experimental Diabetic Neuropathy
Int. J. Mol. Sci. 2022, 23(9), 4887; https://doi.org/10.3390/ijms23094887 - 28 Apr 2022
Cited by 1 | Viewed by 2359
Abstract
Axon degeneration in diabetic peripheral neuropathy (DPN) is associated with impaired NAD+ metabolism. We tested whether the administration of NAD+ precursors, nicotinamide mononucleotide (NMN) or nicotinamide riboside (NR), prevents DPN in models of Type 1 and Type 2 diabetes. NMN was [...] Read more.
Axon degeneration in diabetic peripheral neuropathy (DPN) is associated with impaired NAD+ metabolism. We tested whether the administration of NAD+ precursors, nicotinamide mononucleotide (NMN) or nicotinamide riboside (NR), prevents DPN in models of Type 1 and Type 2 diabetes. NMN was administered to streptozotocin (STZ)-induced diabetic rats and STZ-induced diabetic mice by intraperitoneal injection at 50 or 100 mg/kg on alternate days for 2 months. mice The were fed with a high fat diet (HFD) for 2 months with or without added NR at 150 or 300 mg/kg for 2 months. The administration of NMN to STZ-induced diabetic rats or mice or dietary addition of NR to HFD-fed mice improved sensory function, normalized sciatic and tail nerve conduction velocities, and prevented loss of intraepidermal nerve fibers in skin samples from the hind-paw. In adult dorsal root ganglion (DRG) neurons isolated from HFD-fed mice, there was a decrease in NAD+ levels and mitochondrial maximum reserve capacity. These impairments were normalized in isolated DRG neurons from NR-treated mice. The results indicate that the correction of NAD+ depletion in DRG may be sufficient to prevent DPN but does not significantly affect glucose tolerance, insulin levels, or insulin resistance. Full article
(This article belongs to the Special Issue Metabolic Syndrome: From Molecular Mechanisms to Novel Therapies 2.0)
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Review

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Review
The Role of PKC-MAPK Signalling Pathways in the Development of Hyperglycemia-Induced Cardiovascular Complications
Int. J. Mol. Sci. 2022, 23(15), 8582; https://doi.org/10.3390/ijms23158582 - 02 Aug 2022
Cited by 2 | Viewed by 1449
Abstract
Cardiovascular disease is the most common cause of death among diabetic patients worldwide. Hence, cardiovascular wellbeing in diabetic patients requires utmost importance in disease management. Recent studies have demonstrated that protein kinase C activation plays a vital role in the development of cardiovascular [...] Read more.
Cardiovascular disease is the most common cause of death among diabetic patients worldwide. Hence, cardiovascular wellbeing in diabetic patients requires utmost importance in disease management. Recent studies have demonstrated that protein kinase C activation plays a vital role in the development of cardiovascular complications via its activation of mitogen-activated protein kinase (MAPK) cascades, also known as PKC-MAPK pathways. In fact, persistent hyperglycaemia in diabetic conditions contribute to preserved PKC activation mediated by excessive production of diacylglycerol (DAG) and oxidative stress. PKC-MAPK pathways are involved in several cellular responses, including enhancing oxidative stress and activating signalling pathways that lead to uncontrolled cardiac and vascular remodelling and their subsequent dysfunction. In this review, we discuss the recent discovery on the role of PKC-MAPK pathways, the mechanisms involved in the development and progression of diabetic cardiovascular complications, and their potential as therapeutic targets for cardiovascular management in diabetic patients. Full article
(This article belongs to the Special Issue Metabolic Syndrome: From Molecular Mechanisms to Novel Therapies 2.0)
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Review
New Insights into the Role of Insulin and Hypothalamic-Pituitary-Adrenal (HPA) Axis in the Metabolic Syndrome
Int. J. Mol. Sci. 2022, 23(15), 8178; https://doi.org/10.3390/ijms23158178 - 25 Jul 2022
Viewed by 3975
Abstract
Recent data suggests that (pre)diabetes onset is preceded by a period of hyperinsulinemia. Consumption of the “modern” Western diet, over-nutrition, genetic background, decreased hepatic insulin clearance, and fetal/metabolic programming may increase insulin secretion, thereby causing chronic hyperinsulinemia. Hyperinsulinemia is an important etiological factor [...] Read more.
Recent data suggests that (pre)diabetes onset is preceded by a period of hyperinsulinemia. Consumption of the “modern” Western diet, over-nutrition, genetic background, decreased hepatic insulin clearance, and fetal/metabolic programming may increase insulin secretion, thereby causing chronic hyperinsulinemia. Hyperinsulinemia is an important etiological factor in the development of metabolic syndrome, type 2 diabetes, cardiovascular disease, polycystic ovarian syndrome, and Alzheimer’s disease. Recent data suggests that the onset of prediabetes and diabetes are preceded by a variable period of hyperinsulinemia. Emerging data suggest that chromic hyperinsulinemia is also a driving force for increased activation of the hypothalamic-adrenal-pituitary (HPA) axis in subjects with the metabolic syndrome, leading to a state of “functional hypercortisolism”. This “functional hypercortisolism” by antagonizing insulin actions may prevent hypoglycemia. It also disturbs energy balance by shifting energy fluxes away from muscles toward abdominal fat stores. Synergistic effects of hyperinsulinemia and “functional hypercortisolism” promote abdominal visceral obesity and insulin resistance which are core pathophysiological components of the metabolic syndrome. It is hypothesized that hyperinsulinemia-induced increased activation of the HPA axis plays an important etiological role in the development of the metabolic syndrome and its consequences. Numerous studies have demonstrated reversibility of hyperinsulinemia with lifestyle, surgical, and pharmaceutical-based therapies. Longitudinal studies should be performed to investigate whether strategies that reduce hyperinsulinemia at an early stage are successfully in preventing increased activation of the HPA axis and the metabolic syndrome. Full article
(This article belongs to the Special Issue Metabolic Syndrome: From Molecular Mechanisms to Novel Therapies 2.0)
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