Mechanisms involved in developmental programming of hypertension and renal diseases. Gender differences

2014 ◽  
Vol 18 (2) ◽  
Author(s):  
Analia Lorena Tomat ◽  
Francisco Javier Salazar
Keyword(s):  
Metabolic Diseases ◽  
Current Knowledge ◽  
Adult Life ◽  
Developmental Programming ◽  
Renal Diseases ◽  
Future Studies ◽  
Functional Changes ◽  
Regulatory Systems ◽  
Increased Risk ◽  
Renal Changes

AbstractA substantial body of epidemiological and experimental evidence suggests that a poor fetal and neonatal environment may “program” susceptibility in the offspring to later development of cardiovascular, renal and metabolic diseases.This review focuses on current knowledge from the available literature regarding the mechanisms linking an adverse developmental environment with an increased risk for cardiovascular, renal and metabolic diseases in adult life. Moreover, this review highlights important sex-dependent differences in the adaptation to developmental insults.Developmental programming of several diseases is secondary to changes in different mechanisms inducing important alterations in the normal development of several organs that lead to significant changes in birth weight. The different diseases occurring as a consequence of an adverse environment during development are secondary to morphological and functional cardiovascular and renal changes, to epigenetic changes and to an activation of several hormonal and regulatory systems, such as angiotensin II, sympathetic activity, nitric oxide, COX2-derived metabolites, oxidative stress and inflammation. The important sex-dependent differences in the developmental programming of diseases seem to be partly secondary to the effects of sex hormones. Recent studies have shown that the progression of these diseases is accelerated during aging in both sexes.The cardiovascular, renal and metabolic diseases during adult life that occur as a consequence of several insults during fetal and postnatal periods are secondary to multiple structural and functional changes. Future studies are needed in order to prevent the origin and reduce the incidence and consequences of developmental programmed diseases.

Birth order is associated with an increased risk of obesity in young adults in Thailand

2020 ◽  
pp. jech-2019-213572
Author(s):  
Linda Aurpibul ◽  
Éadaoin M Butler ◽  
Antika Wongthanee ◽  
Amaraporn Rerkasem ◽  
Sakda Pruenglampoo ◽  
...  
Keyword(s):  
Young Adults ◽  
Birth Order ◽  
Metabolic Diseases ◽  
Adult Life ◽  
Intima Media Thickness ◽  
Birth Cohort Study ◽  
Maternal Body Mass Index ◽  
Adjusted Relative Risk ◽  
Model Assessment ◽  
Increased Risk

BackgroundThere is a growing body of evidence showing that early life events are associated with increased risk of cardiovascular and metabolic diseases later in adult life. However, there is a paucity of data in this field from Asian populations. In this study, we examined the association of birth order with obesity risk and cardiometabolic outcomes in young adults in Thailand.MethodsParticipants were the offspring from a birth cohort study in Chiang Mai (northern Thailand), who were followed up at ~20.5 years of age. Clinical assessments included anthropometry, blood pressure, fasting blood samples and carotid intima-media thickness. Insulin sensitivity was estimated using homeostatic model assessment of insulin resistance (HOMA-IR). Participants were stratified into two groups: first-borns and later-borns. Health outcomes between groups were compared using multivariable models adjusting for important confounders, in particular maternal body mass index (BMI).ResultsA total of 559 participants were studied: 316 first-borns (46% males) and 243 later-borns (47% males). Adjusted models showed anthropometric differences, with first-borns being 2.3 kg heavier (p=0.023) with a BMI 0.86 kg/m2 greater (p=0.019) than later-borns. Thus, rates of obesity were higher in first-borns than in later-borns (6.6% vs 2.9%), so that first-borns had an adjusted relative risk of obesity 3.3 times greater than later-borns [95% CI 1.42 to 7.88; p=0.006]. There were no observed differences in cardiovascular or metabolic parameters assessed, including HOMA-IR.ConclusionAs observed in other populations, first-borns in Thailand had greater BMI and an increased risk of obesity in young adulthood. However, we observed no other cardiometabolic differences between first- and later-borns.

scholarly journals Effects of hyperthyroidism on bone mass in women of reproductive age

2004 ◽  
Vol 57 (3-4) ◽  
pp. 111-115
Author(s):  
Jana Ilic ◽  
Branka Kovacev ◽  
Ljiljana Todorovic-Djilas
Keyword(s):  
Bone Mass ◽  
Adult Life ◽  
Reproductive Age ◽  
Control Group ◽  
Mineral Density ◽  
Women Of Reproductive Age ◽  
Anthropometric Parameters ◽  
Future Studies ◽  
Catabolic Rate ◽  
Increased Risk

Introduction Hyperthyroidism is one of the most frequent endocrinopathies in women of reproductive age. Consequently, increased risk of osteoporosis may be expected. Material and methods The research has included a group of 30 hyperthyroid women and a control group of 30 healthy women of reproductive age. Age and some clinical characteristics were analyzed, as well as some anthropometric parameters. Bone mass parameters were determined by measuring bone mineral density using ultrasound devices (SAHARA-Hologic). Results Bone mass parameters in hyperthyroid women are significantly lower than in controls (BUA: 63.25?12.17; 69.73?10.02 dB/MHz respectively; SOS:1523.90? 24.47; 1540.19?26.59 m/s respec. QUI/STIFF 79.78?13.95; 89.09?13.99 % respec.) Duration of hyperthyroidism affects bone density and reduces it. Discussion Obtained results were expected, having in mind that hyper- thyroidism is a condition characterized by increased bone catabolic rate. Also, negative correlation between the duration of hyperthyroidism and bone mass parameters (BUA, SOS) was expected, because it is logical that consolidation of bone mass in adult life cannot be maintained in circumstances in which metabolic rate is increased. During hyperthyroidism, bone loss is expected. In order to confirm this, future studies of bone markers are necessary. Conclusion Based on results obtained in the study, the following conclusions were made: hyperthyroidism is accompanied by decreased values of bone mass parameters; this effect depends on duration of hyperthyroidism. We confirmed that hyperthyroidism may be the cause of decrease in bone mass, particularly if it lasts more than a year. To prevent osteoporosis in women of reproductive age with hyperthyroidism and involution osteoporosis later in life, early diagnosis and effective therapy of hyperthyroidism is imperative.

scholarly journals Matrix Metalloproteinases in Renal Diseases: A Critical Appraisal

2019 ◽  
Vol 44 (3) ◽  
pp. 298-330 ◽  
Author(s):  
Oskar Zakiyanov ◽  
Marta Kalousová ◽  
Tomáš Zima ◽  
Vladimír Tesař
Keyword(s):  
Matrix Metalloproteinases ◽  
Animal Studies ◽  
Critical Appraisal ◽  
Current Knowledge ◽  
Kidney Diseases ◽  
Tissue Inhibitors Of Metalloproteinases ◽  
Renal Diseases ◽  
Tubular Epithelial Cells ◽  
Renal Changes ◽  
Membrane Type

Matrix metalloproteinases (MMPs) are endopeptidases within the metzincin protein family that not only cleave extracellular matrix (ECM) components, but also process the non-ECM molecules, including various growth factors and their binding proteins. MMPs participate in cell to ECM interactions, and MMPs are known to be involved in cell proliferation mechanisms and most probably apoptosis. These proteinases are grouped into six classes: collagenases, gelatinases, stromelysins, matrilysins, membrane type MMPs, and other MMPs. Various mechanisms regulate the activity of MMPs, inhibition by tissue inhibitors of metalloproteinases being the most important. In the kidney, intrinsic glomerular cells and tubular epithelial cells synthesize several MMPs. The measurement of circulating MMPs can provide valuable information in patients with kidney diseases. They play an important role in many renal diseases, both acute and chronic. This review attempts to summarize the current knowledge of MMPs in the kidney and discusses recent data from patient and animal studies with reference to specific diseases. A better understanding of the MMPs’ role in renal remodeling may open the way to new interventions favoring deleterious renal changes in a number of kidney diseases.

Mesophyll conductance: the leaf corridors for photosynthesis

2020 ◽  
Vol 48 (2) ◽  
pp. 429-439 ◽  
Author(s):  
Jorge Gago ◽  
Danilo M. Daloso ◽  
Marc Carriquí ◽  
Miquel Nadal ◽  
Melanie Morales ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Main Role ◽  
Mesophyll Conductance ◽  
Future Studies ◽  
Cell Structures ◽  
Leaf Tissues ◽  
Change Framework ◽  
Chloroplast Stroma

Besides stomata, the photosynthetic CO2 pathway also involves the transport of CO2 from the sub-stomatal air spaces inside to the carboxylation sites in the chloroplast stroma, where Rubisco is located. This pathway is far to be a simple and direct way, formed by series of consecutive barriers that the CO2 should cross to be finally assimilated in photosynthesis, known as the mesophyll conductance (gm). Therefore, the gm reflects the pathway through different air, water and biophysical barriers within the leaf tissues and cell structures. Currently, it is known that gm can impose the same level of limitation (or even higher depending of the conditions) to photosynthesis than the wider known stomata or biochemistry. In this mini-review, we are focused on each of the gm determinants to summarize the current knowledge on the mechanisms driving gm from anatomical to metabolic and biochemical perspectives. Special attention deserve the latest studies demonstrating the importance of the molecular mechanisms driving anatomical traits as cell wall and the chloroplast surface exposed to the mesophyll airspaces (Sc/S) that significantly constrain gm. However, even considering these recent discoveries, still is poorly understood the mechanisms about signaling pathways linking the environment a/biotic stressors with gm responses. Thus, considering the main role of gm as a major driver of the CO2 availability at the carboxylation sites, future studies into these aspects will help us to understand photosynthesis responses in a global change framework.

Plant Compounds for the Treatment of Diabetes, a Metabolic Disorder: NF-κB as a Therapeutic Target

2020 ◽  
Vol 26 (39) ◽  
pp. 4955-4969
Author(s):  
Ravi Sahukari ◽  
Jyothi Punabaka ◽  
Shanmugam Bhasha ◽  
Venkata S. Ganjikunta ◽  
Shanmugam K. Ramudu ◽  
...  
Keyword(s):  
Diabetic Complications ◽  
Current Knowledge ◽  
World Population ◽  
Future Studies ◽  
Expression Of Genes ◽  
Treatment Of Diabetes ◽  
Online Library ◽  
And Oxidative Stress ◽  
Stress Activation ◽  
Plant Compounds

Background: The prevalence of diabetes in the world population hás reached 8.8 % and is expected to rise to 10.4% by 2040. Hence, there is an urgent need for the discovery of drugs against therapeutic targets to sojourn its prevalence. Previous studies proved that NF-κB serves as a central agent in the development of diabetic complications. Objectives: This review intended to list the natural plant compounds that would act as inhibitors of NF-κB signalling in different organs under the diabetic condition with their possible mechanism of action. Methods: Information on NF-κB, diabetes, natural products, and relation in between them, was gathered from scientific literature databases such as Pubmed, Medline, Google scholar, Science Direct, Springer, Wiley online library. Results and Conclusion: NF-κB plays a crucial role in the development of diabetic complications because of its link in the expression of genes that are responsible for organs damage such as kidney, brain, eye, liver, heart, muscle, endothelium, adipose tissue and pancreas by inflammation, apoptosis and oxidative stress. Activation of PPAR-α, SIRT3/1, and FXR through many cascades by plant compounds such as terpenoids, iridoids, flavonoids, alkaloids, phenols, tannins, carbohydrates, and phytocannabinoids recovers diabetic complications. These compounds also exhibit the prevention of NF-κB translocation into the nucleus by inhibiting NF-κB activators, such as VEGFR, RAGE and TLR4 receptors, which in turn, prevent the activation of many genes involved in tissue damage. Current knowledge on the treatment of diabetes by targeting NF-κB is limited, so future studies would enlighten accordingly.

Cardiovascular Complications in Patients with Klinefelter’s Syndrome

2020 ◽  
Vol 26 (43) ◽  
pp. 5556-5563
Author(s):  
Franz Sesti ◽  
Riccardo Pofi ◽  
Carlotta Pozza ◽  
Marianna Minnetti ◽  
Daniele Gianfrilli ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Klinefelter Syndrome ◽  
Subclinical Atherosclerosis ◽  
Cardiovascular Complications ◽  
High Risk Population ◽  
Metabolic Disturbances ◽  
Future Studies ◽  
Increased Risk ◽  
Chromosome Disorder

More than 70 years have passed since the first description of Klinefelter Syndrome (KS), the most frequent chromosome disorder causing male infertility and hypogonadism. KS is associated with increased cardiovascular (CV) mortality due to several comorbidities, including hypogonadism, as well as metabolic syndrome and type 2 diabetes, which are highly prevalent in these patients. Aside from metabolic disturbances, patients with KS suffer from both acquired and congenital CV abnormalities, cerebrovascular thromboembolic disease, subclinical atherosclerosis and endothelial dysfunction, which may all contribute to increased CV mortality. The mechanisms involved in this increased risk of CV morbidity and mortality are not entirely understood. More research is needed to better characterise the CV manifestations, elucidate the pathophysiological mechanisms and define the contribution of testosterone replacement to restoring CV health in KS patients. This review explores the complex association between KS, metabolic syndrome and CV risk in order to plan future studies and improve strategies to reduce mortality in this high-risk population.

scholarly journals Epilepsy in Down Syndrome: A Highly Prevalent Comorbidity

2021 ◽  
Vol 10 (13) ◽  
pp. 2776
Author(s):  
Miren Altuna ◽  
Sandra Giménez ◽  
Juan Fortea
Keyword(s):  
Down Syndrome ◽  
Functional Outcomes ◽  
Clinical Presentation ◽  
Late Onset ◽  
Current Knowledge ◽  
Epileptic Seizures ◽  
Myoclonic Epilepsy ◽  
Increased Risk ◽  
Number Of Individuals

Individuals with Down syndrome (DS) have an increased risk for epilepsy during the whole lifespan, but especially after age 40 years. The increase in the number of individuals with DS living into late middle age due to improved health care is resulting in an increase in epilepsy prevalence in this population. However, these epileptic seizures are probably underdiagnosed and inadequately treated. This late onset epilepsy is linked to the development of symptomatic Alzheimer’s disease (AD), which is the main comorbidity in adults with DS with a cumulative incidence of more than 90% of adults by the seventh decade. More than 50% of patients with DS and AD dementia will most likely develop epilepsy, which in this context has a specific clinical presentation in the form of generalized myoclonic epilepsy. This epilepsy, named late onset myoclonic epilepsy (LOMEDS) affects the quality of life, might be associated with worse cognitive and functional outcomes in patients with AD dementia and has an impact on mortality. This review aims to summarize the current knowledge about the clinical and electrophysiological characteristics, diagnosis and treatment of epileptic seizures in the DS population, with a special emphasis on LOMEDS. Raised awareness and a better understanding of epilepsy in DS from families, caregivers and clinicians could enable earlier diagnoses and better treatments for individuals with DS.

scholarly journals The relevance of adhesion G protein-coupled receptors in metabolic functions

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Isabell Kaczmarek ◽  
Tomáš Suchý ◽  
Simone Prömel ◽  
Torsten Schöneberg ◽  
Ines Liebscher ◽  
...  
Keyword(s):  
G Protein ◽  
Drug Targets ◽  
Metabolic Diseases ◽  
Current Knowledge ◽  
G Protein Coupled Receptors ◽  
Specific Expression ◽  
Physiological Functions ◽  
Metabolic Functions ◽  
Central Nervous Systems ◽  
G Protein Coupled

Abstract G protein-coupled receptors (GPCRs) modulate a variety of physiological functions and have been proven to be outstanding drug targets. However, approximately one-third of all non-olfactory GPCRs are still orphans in respect to their signal transduction and physiological functions. Receptors of the class of Adhesion GPCRs (aGPCRs) are among these orphan receptors. They are characterized by unique features in their structure and tissue-specific expression, which yields them interesting candidates for deorphanization and testing as potential therapeutic targets. Capable of G-protein coupling and non-G protein-mediated function, aGPCRs may extend our repertoire of influencing physiological function. Besides their described significance in the immune and central nervous systems, growing evidence indicates a high importance of these receptors in metabolic tissue. RNAseq analyses revealed high expression of several aGPCRs in pancreatic islets, adipose tissue, liver, and intestine but also in neurons governing food intake. In this review, we focus on aGPCRs and their function in regulating metabolic pathways. Based on current knowledge, this receptor class represents high potential for future pharmacological approaches addressing obesity and other metabolic diseases.

scholarly journals Endocannabinoid System Dysregulation from Acetaminophen Use May Lead to Autism Spectrum Disorder: Could Cannabinoid Treatment Be Efficacious?

Molecules ◽  
2021 ◽  
Vol 26 (7) ◽  
pp. 1845
Author(s):  
Stephen Schultz ◽  
Georgianna G. Gould ◽  
Nicola Antonucci ◽  
Anna Lisa Brigida ◽  
Dario Siniscalco
Keyword(s):  
Autism Spectrum Disorder ◽  
Cannabinoid Receptors ◽  
Current Knowledge ◽  
Endocannabinoid System ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Blood Levels ◽  
Increased Risk ◽  
Patterns Of Behavior ◽  
Arachidonoyl Glycerol

Persistent deficits in social communication and interaction, and restricted, repetitive patterns of behavior, interests or activities, are the core items characterizing autism spectrum disorder (ASD). Strong inflammation states have been reported to be associated with ASD. The endocannabinoid system (ECS) may be involved in ASD pathophysiology. This complex network of lipid signaling pathways comprises arachidonic acid and 2-arachidonoyl glycerol-derived compounds, their G-protein-coupled receptors (cannabinoid receptors CB1 and CB2) and the associated enzymes. Alterations of the ECS have been reported in both the brain and the immune system of ASD subjects. ASD children show low EC tone as indicated by low blood levels of endocannabinoids. Acetaminophen use has been reported to be associated with an increased risk of ASD. This drug can act through the ECS to produce analgesia. It may be that acetaminophen use in children increases the risk for ASD by interfering with the ECS.This mini-review article summarizes the current knowledge on this topic.

scholarly journals Urinary Extracellular Vesicles for Diabetic Kidney Disease Diagnosis

2021 ◽  
Vol 10 (10) ◽  
pp. 2046
Author(s):  
Goren Saenz-Pipaon ◽  
Saioa Echeverria ◽  
Josune Orbe ◽  
Carmen Roncal
Keyword(s):  
Kidney Disease ◽  
Extracellular Vesicles ◽  
Diabetic Kidney Disease ◽  
Current Knowledge ◽  
Developed Countries ◽  
Disease Diagnosis ◽  
Renal Diseases ◽  
Diabetic Kidney ◽  
Glucose Levels ◽  
Stage Renal Disease

Diabetic kidney disease (DKD) is the leading cause of end stage renal disease (ESRD) in developed countries, affecting more than 40% of diabetes mellitus (DM) patients. DKD pathogenesis is multifactorial leading to a clinical presentation characterized by proteinuria, hypertension, and a gradual reduction in kidney function, accompanied by a high incidence of cardiovascular (CV) events and mortality. Unlike other diabetes-related complications, DKD prevalence has failed to decline over the past 30 years, becoming a growing socioeconomic burden. Treatments controlling glucose levels, albuminuria and blood pressure may slow down DKD evolution and reduce CV events, but are not able to completely halt its progression. Moreover, one in five patients with diabetes develop DKD in the absence of albuminuria, and in others nephropathy goes unrecognized at the time of diagnosis, urging to find novel noninvasive and more precise early diagnosis and prognosis biomarkers and therapeutic targets for these patient subgroups. Extracellular vesicles (EVs), especially urinary (u)EVs, have emerged as an alternative for this purpose, as changes in their numbers and composition have been reported in clinical conditions involving DM and renal diseases. In this review, we will summarize the current knowledge on the role of (u)EVs in DKD.

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