scholarly journals Cyanidin-3-O-glucoside inhibits different enzymes involved in central nervous system pathologies and type-2 diabetes

2019 ◽  
Vol 120 ◽  
pp. 241-246 ◽  
Author(s):  
Guillermo Cásedas ◽  
Francisco Les ◽  
Elena González-Burgos ◽  
Maria Pilar Gómez-Serranillos ◽  
Carine Smith ◽  
...  
2016 ◽  
Vol 18 (4) ◽  
pp. 415-424 ◽  

One of the most sexually dimorphic aspects of metabolic regulation is the bidirectional modulation of glucose and energy homeostasis by testosterone in males and females. Testosterone deficiency predisposes men to metabolic dysfunction, with excess adiposity, insulin resistance, and type 2 diabetes, whereas androgen excess predisposes women to insulin resistance, adiposity, and type 2 diabetes. This review discusses how testosterone acts in the central nervous system, and especially the hypothalamus, to promote metabolic homeostasis or dysfunction in a sexually dimorphic manner. We compare the organizational actions of testosterone, which program the hypothalamic control of metabolic homeostasis during development, and the activational actions of testosterone, which affect metabolic function after puberty. We also discuss how the metabolic effect of testosterone is centrally mediated via the androgen receptor.


2010 ◽  
Vol 1 (1) ◽  
pp. 31 ◽  
Author(s):  
PeterJ Jannetta ◽  
LynnH Fletcher ◽  
PeterM Grondziowski ◽  
KennethF Casey ◽  
RaymondF Sekula

2020 ◽  
Author(s):  
Arthur T. Kopylov ◽  
Olga Papysheva ◽  
Iveta Gribova ◽  
Anna L. Kaysheva ◽  
Galina Kotaysch ◽  
...  

Abstract Background Maternal diabetes either pregestational or gestational is the main risk factor contributing in development of diabetic fetopathy (DF) in newborns. There are no generalized signs of DF up to late gestational age due to insufficient sensitivity of the currently employed instrumental methods for diagnosis. Methods This is a cross-sectional prospective controlled study. Here, we reported proteomic investigation for several cases of severe types of diabetic fetopathy (cardiomyopathy (CRDM, n = 37), central nervous system depression (CNSD, n = 35) and hepatomegaly (HPMG, n = 35)) diagnosed during 30–35 gestational weeks and confirmed upon delivery by from patients with type 2 diabetes mellitus (T2DM). Control groups were comprised from women in whom T2DM had been ruled out (n = 40) and group of pregnancies with T2DM who delivered healthy newborns (n = 40). Results We found a composition of serum-based non-trivial markers capable that are strongly associated with the certain type of fetopathy or anatomical malfunctions in the affected newborns. Significant impact on mRNA splicing and DNA reparation has been determined by emerging alterations in CDCL5. Patients of CNSD groups were characterized by utmost depletion (ca. 7% of baseline) of DFP3 neurotrophic factor needed for the proper specialization of cardiomyocytes and oligodendrocytes. Corrupted regulation of non-canonical Wnt-signaling guided by PEDF (in CNSD and HPMG groups) and DAAM2 (in CRDM and HPMG groups) was also proposed. In addition, deficiency in retinoic acid and thyroxine transport was revealed by dramatic increase of TTHY in CNDS group. Conclusions We examined peripheral blood plasma and determined a small proportion of proteins indicating the pre-existing signs of DF. Most of the examined markers are participants of critical processes at different stages of embryogenesis and regulate various phases of morphogenesis. There are proteins regulating splicing and DNA repair, differentiation of neurons and their switching to the post-mitotic state. Therefore, reconstruction of the molecular interplay between the defined in proteins is decisive to appreciate cryptic violations in fetal development on the background of diabetic conditions


2020 ◽  
Vol 40 (4) ◽  
pp. 1499-1511
Author(s):  
José Alfredo Padilla Medina ◽  
Carlos Alonso Herrera Ramírez ◽  
Luz María Cardona Torres ◽  
Delia Angélica Galicia Reséndiz ◽  
Juan Prado Olivares ◽  
...  

Author(s):  
Zaman Mirzadeh ◽  
Chelsea L. Faber ◽  
Michael W. Schwartz

Historically, pancreatic islet beta cells have been viewed as principal regulators of glycemia, with type 2 diabetes (T2D) resulting when insulin secretion fails to compensate for peripheral tissue insulin resistance. However, glycemia is also regulated by insulin-independent mechanisms that are dysregulated in T2D. Based on evidence supporting its role both in adaptive coupling of insulin secretion to changes in insulin sensitivity and in the regulation of insulin-independent glucose disposal, the central nervous system (CNS) has emerged as a fundamental player in glucose homeostasis. Here, we review and expand upon an integrative model wherein the CNS, together with the islet, establishes and maintains the defended level of glycemia. We discuss the implications of this model for understanding both normal glucose homeostasis and T2D pathogenesis and highlight centrally targeted therapeutic approaches with the potential to restore normoglycemia to patients with T2D.


2012 ◽  
Vol 97 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Rory J. McCrimmon

Hypoglycemia remains a major clinical issue in the management of people with type 1 and type 2 diabetes. Research in basic science is only beginning to unravel the mechanisms that: 1) underpin the detection of hypoglycemia and initiation of a counterregulatory defense response; and 2) contribute to the development of defective counterregulation in both type 1 and type 2 diabetes, particularly after prior exposure to repeated hypoglycemia. In animal studies, the central nervous system has emerged as key to these processes. However, bench-based research needs to be translated through studies in human subjects as a first step to the future development of clinical intervention. This Update reviews studies published in the last 2 yr that examined the central nervous system effects of hypoglycemia in human subjects, largely through neuroimaging techniques, and compares these data with those obtained from animal studies and the implications for future therapies. Based on these studies, it is increasingly clear that our understanding of how the brain responds and adapts to recurrent hypoglycemia remains very limited. Current therapies have provided little evidence that they can prevent severe hypoglycemia or improve hypoglycemia awareness in type 1 diabetes. There remains an urgent need to increase our understanding of how and why defective counterregulation develops in type 1 diabetes in order for novel therapeutic interventions to be developed and tested.


Author(s):  
Yu. Urmanova ◽  
A. Holikov

THE PURPOSE OF THE STUDY is to carry out an analysis of the literature evaluating diabetic encephalopathy by determining neuromarkers. MATERIAL AND METHODS. In this article, the authors analyzed the literature on the role of neuromarkers in patients with type 2 diabetes mellitus undergoing program hemodialysis. RESEARCH RESULTS. Among biochemical markers, the determination of the level of neurospecific proteins is actively being investigated. The main part of them is autoantigens, entering the bloodstream, can cause the appearance of autoantibodies, which, when the blood-brain barrier is impaired, enter the brain from the blood vessel and cause morphological changes, destructive processes in neurons, as well as the development of nonspecific acute-phase reactions like edema or inflammation. Biomarker studies for the diagnosis of various brain lesions have been under way for more than 20 years, but at present no ideal biomarker has been found. Among biochemical markers, the determination of the level of neurospecific proteins is being actively studied. In patients with type 2 diabetes mellitus undergoing hemodialysis, this issue is also relevant in view of the frequent vascular cerebrovascular complications, but few studies have been conducted. CONCLUSIONS. All of the above emphasizes the need to identify the features of clinical and functional changes in the nervous system in patients with type 2 diabetes mellitus receiving program hemodialysis and to evaluate the prognostic value of neuromarkers in early detection of the degree of brain damage. 


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