scholarly journals The Role of Autophagy in Liver Epithelial Cells and Its Impact on Systemic Homeostasis

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 827 ◽  
Author(s):  
Tomaipitinca ◽  
Mandatori ◽  
Mancinelli ◽  
Giulitti ◽  
Petrungaro ◽  
...  
Keyword(s):  
Plasma Proteins ◽  
Hepatic Metabolism ◽  
Toxic Substances ◽  
The Metabolic Syndrome ◽  
Liver Functions ◽  
Glucose Storage ◽  
Muscle Homeostasis ◽  
Cellular Components ◽  
Bile Production

: Autophagy plays a role in several physiological and pathological processes as it controls the turnover rate of cellular components and influences cellular homeostasis. The liver plays a central role in controlling organisms’ metabolism, regulating glucose storage, plasma proteins and bile synthesis and the removal of toxic substances. Liver functions are particularly sensitive to autophagy modulation. In this review we summarize studies investigating how autophagy influences the hepatic metabolism, focusing on fat accumulation and lipids turnover. We also describe how autophagy affects bile production and the scavenger function within the complex homeostasis of the liver. We underline the role of hepatic autophagy in counteracting the metabolic syndrome and the associated cardiovascular risk. Finally, we highlight recent reports demonstrating how the autophagy occurring within the liver may affect skeletal muscle homeostasis as well as different extrahepatic solid tumors, such as melanoma.

Role of genetic factors in the development of hypertension in young patients with metabolic syndrome

2020 ◽  
pp. 23-32
Author(s):  
Elena Korneeva ◽  
Mikhail Voevoda ◽  
Sergey Semaev ◽  
Vladimir Maksimov
Keyword(s):  
Metabolic Syndrome ◽  
High Risk ◽  
Arterial Hypertension ◽  
Genetic Factors ◽  
Young Patients ◽  
Integrin Αiibβ3 ◽  
Ace Gene ◽  
The Metabolic Syndrome

Results of the study related to polymorphism of ACE gene (rs1799752)‎, integrin αIIbβ3, and CSK gene (rs1378942) influencing development of arterial hypertension in young patients with metabolic syndrome are presented. Hypertension as a component of the metabolic syndrome was detected in 15.0% of young patients. Prevalence of mutant alleles of the studied genes among the examined patients was quite high, so homozygous DD genotype was found in 21.6%, and mutant D allele of the ACE gene in 47.4%. A high risk of hypertension in patients with MS was detected in carriers of the T allele of the CSK (rs1378942) gene – 54.8%, which was most often observed in a combination of polymorphic ACE and CSK gene loci (p = 0.0053).

Cubilin, the Intrinsic Factor-Vitamin B12 Receptor in Development and Disease

2020 ◽  
Vol 27 (19) ◽  
pp. 3123-3150 ◽  
Author(s):  
Renata Kozyraki ◽  
Olivier Cases
Keyword(s):  
Vitamin B12 ◽  
Cancer Progression ◽  
Intrinsic Factor ◽  
Basic Research ◽  
Toxic Substances ◽  
Human Pathology ◽  
Peripheral Membrane Protein ◽  
Epidermal Growth ◽  
Fgf8 Signaling

Gp280/Intrinsic factor-vitamin B12 receptor/Cubilin (CUBN) is a large endocytic receptor serving multiple functions in vitamin B12 homeostasis, renal reabsorption of protein or toxic substances including albumin, vitamin D-binding protein or cadmium. Cubilin is a peripheral membrane protein consisting of 8 Epidermal Growth Factor (EGF)-like repeats and 27 CUB (defined as Complement C1r/C1s, Uegf, BMP1) domains. This structurally unique protein interacts with at least two molecular partners, Amnionless (AMN) and Lrp2/Megalin. AMN is involved in appropriate plasma membrane transport of Cubilin whereas Lrp2 is essential for efficient internalization of Cubilin and its ligands. Observations gleaned from animal models with Cubn deficiency or human diseases demonstrate the importance of this protein. In this review addressed to basic research and medical scientists, we summarize currently available data on Cubilin and its implication in renal and intestinal biology. We also discuss the role of Cubilin as a modulator of Fgf8 signaling during embryonic development and propose that the Cubilin-Fgf8 interaction may be relevant in human pathology, including in cancer progression, heart or neural tube defects. We finally provide experimental elements suggesting that some aspects of Cubilin physiology might be relevant in drug design.

scholarly journals Endothelial Dysfunction in Diabetes Is Aggravated by Glycated Lipoproteins; Novel Molecular Therapies

Biomedicines ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 18
Author(s):  
Laura Toma ◽  
Camelia Sorina Stancu ◽  
Anca Volumnia Sima
Keyword(s):  
Plasma Proteins ◽  
Diabetes Complications ◽  
Vascular Complications ◽  
High Density Lipoproteins ◽  
Diabetic Patients ◽  
Inflammatory Stress ◽  
Glycation End Products ◽  
Molecular Therapies ◽  
Specific Receptors

Diabetes and its vascular complications affect an increasing number of people. This disease of epidemic proportion nowadays involves abnormalities of large and small blood vessels, all commencing with alterations of the endothelial cell (EC) functions. Cardiovascular diseases are a major cause of death and disability among diabetic patients. In diabetes, EC dysfunction (ECD) is induced by the pathological increase of glucose and by the appearance of advanced glycation end products (AGE) attached to the plasma proteins, including lipoproteins. AGE proteins interact with their specific receptors on EC plasma membrane promoting activation of signaling pathways, resulting in decreased nitric oxide bioavailability, increased intracellular oxidative and inflammatory stress, causing dysfunction and finally apoptosis of EC. Irreversibly glycated lipoproteins (AGE-Lp) were proven to have an important role in accelerating atherosclerosis in diabetes. The aim of the present review is to present up-to-date information connecting hyperglycemia, ECD and two classes of glycated Lp, glycated low-density lipoproteins and glycated high-density lipoproteins, which contribute to the aggravation of diabetes complications. We will highlight the role of dyslipidemia, oxidative and inflammatory stress and epigenetic risk factors, along with the specific mechanisms connecting them, as well as the new promising therapies to alleviate ECD in diabetes.

scholarly journals Pediatric Antiphospholipid Syndrome: from Pathogenesis to Clinical Management

2021 ◽  
Vol 23 (2) ◽  
Author(s):  
Silvia Rosina ◽  
Cecilia Beatrice Chighizola ◽  
Angelo Ravelli ◽  
Rolando Cimaz
Keyword(s):  
Antiphospholipid Syndrome ◽  
Fluid Phase ◽  
Multiple Organ ◽  
Clinical Settings ◽  
Glycoprotein I ◽  
Long Term Follow Up ◽  
Pediatric Populations ◽  
Cellular Components

Abstract Purpose of Review Elucidating the pathogenic mechanisms mediated by antiphospholipid antibodies (aPL) might exert important clinical implications in pediatric antiphospholipid syndrome (APS). Recent Findings aPL are traditionally regarded as the main pathogenic players in APS, inducing thrombosis via the interaction with fluid-phase and cellular components of coagulation. Recent APS research has focused on the role of β2 glycoprotein I, which bridges innate immunity and coagulation. In pediatric populations, aPL should be screened in appropriate clinical settings, such as thrombosis, multiple-organ dysfunction, or concomitant systemic autoimmune diseases. Children positive for aPL tests often present non-thrombotic non-criteria manifestations or asymptomatic aPL positivity. In utero aPL exposure has been suggested to result in developmental disabilities, warranting long-term follow-up. Summary The knowledge of the multifaceted nature of pediatric APS should be implemented to reduce the risk of underdiagnosing/undertreating this condition. Hopefully, recent pathogenic insights will open new windows of opportunity in the management of pediatric APS.

The Role of Healthcare Professionals in Environmental Health and Fertility Decision-Making

2017 ◽  
Vol 27 (1) ◽  
pp. 28-50 ◽  
Author(s):  
Ellen Sweeney
Keyword(s):  
Decision Making ◽  
Healthcare Professionals ◽  
Endocrine Disrupting Chemicals ◽  
Consumer Products ◽  
Professional Organizations ◽  
Toxic Substances ◽  
Industrial Chemicals ◽  
Fertility Decision ◽  
Guidelines And Recommendations

There is increasing evidence that raises specific concerns about prenatal exposures to toxic substances which makes it necessary to consider everyday exposures to industrial chemicals and toxic substances in consumer products, including endocrine disrupting chemicals. Pregnant women have measurable levels of numerous toxic substances from exposures in their everyday environments, including those which are associated with adverse developmental and reproductive health outcomes. As a result, environmental contexts have begun to influence the decisions women make related to fertility, as well as the formal guidelines and advice provided by healthcare professionals. This article provides an overview of the potential role for obstetricians and gynecologists in educating their patients about the role of toxic substances in fertility decision-making and pregnancy. It explores the emerging guidelines and recommendations from professional organizations and problematizes the limitations of these approaches.

Hepatic metabolism of diclofenac: role of human CYP in the minor oxidative pathways

1999 ◽  
Vol 58 (5) ◽  
pp. 787-796 ◽  
Author(s):  
Roque Bort ◽  
Katherine Macé ◽  
Alan Boobis ◽  
Marı́a-José Gómez-Lechón ◽  
Andrea Pfeifer ◽  
...  
Keyword(s):  
Hepatic Metabolism

The Role of Quinapril in the Presence of a Weight Loss Regimen: Endothelial Function and Markers of Obesity in Patients With the Metabolic Syndrome

2007 ◽  
Vol 10 (4) ◽  
pp. 204-209 ◽  
Author(s):  
Sameer Nagamia ◽  
Anbu Pandian ◽  
Faiz Cheema ◽  
Rama Natarajan ◽  
Qamar A. Khan ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Weight Loss ◽  
Endothelial Function ◽  
The Metabolic Syndrome

scholarly journals Vitamin D signalling in adipose tissue

2012 ◽  
Vol 108 (11) ◽  
pp. 1915-1923 ◽  
Author(s):  
Cherlyn Ding ◽  
Dan Gao ◽  
John Wilding ◽  
Paul Trayhurn ◽  
Chen Bing
Keyword(s):  
Vitamin D ◽  
Adipose Tissue ◽  
Vitamin D Deficiency ◽  
Vitamin D Metabolites ◽  
Hydroxyvitamin D ◽  
The Metabolic Syndrome ◽  
Prevalence Of Obesity ◽  
Adipose Tissue Development ◽  
And Function

Vitamin D deficiency and the rapid increase in the prevalence of obesity are both considered important public health issues. The classical role of vitamin D is in Ca homoeostasis and bone metabolism. Growing evidence suggests that the vitamin D system has a range of physiological functions, with vitamin D deficiency contributing to the pathogenesis of several major diseases, including obesity and the metabolic syndrome. Clinical studies have shown that obese individuals tend to have a low vitamin D status, which may link to the dysregulation of white adipose tissue. Recent studies suggest that adipose tissue may be a direct target of vitamin D. The expression of both the vitamin D receptor and 25-hydroxyvitamin D 1α-hydroxylase (CYP27B1) genes has been shown in murine and human adipocytes. There is evidence that vitamin D affects body fat mass by inhibiting adipogenic transcription factors and lipid accumulation during adipocyte differentiation. Some recent studies demonstrate that vitamin D metabolites also influence adipokine production and the inflammatory response in adipose tissue. Therefore, vitamin D deficiency may compromise the normal metabolic functioning of adipose tissue. Given the importance of the tissue in energy balance, lipid metabolism and inflammation in obesity, understanding the mechanisms of vitamin D action in adipocytes may have a significant impact on the maintenance of metabolic health. In the present review, we focus on the signalling role of vitamin D in adipocytes, particularly the potential mechanisms through which vitamin D may influence adipose tissue development and function.

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