scholarly journals The Kidney-Heart Connection in Obesity

Nephron ◽  
2021 ◽  
pp. 1-5
Author(s):  
Almudena García-Carrasco ◽  
Adriana Izquierdo-Lahuerta ◽  
Gema Medina-Gómez

There is a strong relationship between the kidney and the heart, where if one of these organs fails, so does the other, in the so-called cardiorenal syndrome (CRS). Besides, there are also interactions with the rest of the body leading to a metabolic state that establishes a feedback loop that is perpetuated. The CRS is characterized by hemodynamic changes, activation of neuro-humoral systems, natriuretic peptides, and changes in mineral metabolism. In this scenario, the kidney and heart, connected by a dysfunctional endothelium, inevitably fail. In obesity, this syndrome is exacerbated due to the complications of adipose tissue dysfunction, in the so-called cardiorenal metabolic syndrome (CRMetS). Obesity promotes adipose tissue dysfunction because it exceeds lipid storage capacity and leads to a lipotoxic state, characterized by inflammation, hypertension, insulin resistance and dyslipidemia, oxidative stress, and hyperuricemia, among others, that affect different organs other than the adipose tissue. In addition, the pro-inflammatory gut microbiota present in obese patients releases uremic toxins, contributing to oxidative stress and inflammation, perpetuating and accelerating the progression of this pathology. In this article, we describe the contribution of obesity, the factors and mechanisms implicated in the development of the CRMetS. Despite the great knowledge about the CRS, more research is needed to characterize the CRMetS given the global obesity epidemic.

Author(s):  
O. V. Povarova ◽  
E. A. Gorodetskaya ◽  
E. I. Kalenikova ◽  
O. S. Medvedev

The article presents a modern view of obesity as a chronic inflammation of adipose tissue. Obesity is accompanied by metabolic changes in lipid, protein, carbohydrate, mineral metabolism and disorders in the hormonal function of adipose tissue as an endo- and paracrine organ. At the moment, there are searched the biochemical markers of metabolic disorders of obesity. The obesity-related factors (hyperglycemia, increased lipid levels, insulin resistance, chronic inflammation, hyperleptinemia, endothelial dysfunction, impaired respiratory function of mitochondria, minerals and microelements deficiency) form and increase oxidative stress making it an integral component of the pathogenesis of obesity and possible complications. Given the important role of Q10 coenzyme in antioxidant tissue protection, the authors discuss the relationship of obesity and metabolic disorders to the endogenous levels of Q10 coenzyme and its possible use for pharmacological correction.


2016 ◽  
Vol 231 (3) ◽  
pp. R77-R99 ◽  
Author(s):  
Liping Luo ◽  
Meilian Liu

Adipose tissue plays a central role in regulating whole-body energy and glucose homeostasis through its subtle functions at both organ and systemic levels. On one hand, adipose tissue stores energy in the form of lipid and controls the lipid mobilization and distribution in the body. On the other hand, adipose tissue acts as an endocrine organ and produces numerous bioactive factors such as adipokines that communicate with other organs and modulate a range of metabolic pathways. Moreover, brown and beige adipose tissue burn lipid by dissipating energy in the form of heat to maintain euthermia, and have been considered as a new way to counteract obesity. Therefore, adipose tissue dysfunction plays a prominent role in the development of obesity and its related disorders such as insulin resistance, cardiovascular disease, diabetes, depression and cancer. In this review, we will summarize the recent findings of adipose tissue in the control of metabolism, focusing on its endocrine and thermogenic function.


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Masayuki Sugimoto ◽  
Hidenori Arai ◽  
Yukinori Tamura ◽  
Toshinori Murayama ◽  
Koh Ono ◽  
...  

Mulberry leaf (ML) is commonly used to feed silkworms. Previous study showed that ML ameliorates atherosclerosis. However, its mechanism is not completely understood. Because dysregulated production of adipocytokines is involved in the development of the metabolic syndrome and cardiovascular disease, we examined the effect of ML on the production of adipocytokines and metabolic disorders related to the metabolic syndrome, and compared its effect with that of a PPARγ agonist, pioglitazone (Pio). By treating obese diabetic db/db mice with ML, Pio, and their combination, we investigated the mechanism by which they improve metabolic disorders. In this study, db/+m (lean control) and db/db mice were fed a standard diet with or without 3% (w/w) ML and/or 0.01% (w/w) Pio for 12 weeks from 9 weeks of age. At the end of the experiment we found that ML decreased plasma glucose and triglyceride by 32% and 30%, respectively. Interestingly, administration of ML in addition to Pio showed additive effects; further 40% and 30% reduction in glucose and triglyceride compared with Pio treatment, respectively. Moreover, administration of ML in addition to Pio suppressed the body weight increase by Pio treatment and reduced visceral/subcutaneous fat ratio by 20% compared with control db/db mice. Importantly, ML treatment increased expression of adiponectin in white adipose tissue (WAT) by 40%, which was only found in db/db mice, not in control db/+m mice. Combination of ML and Pio increased plasma adiponectin concentrations by 25% and its expression in WAT by 17% compared with Pio alone. In contrast, ML decreased expression of TNF-α and MCP-1 by 25% and 20%, respectively, and the addition of Pio resulted in a further decrease of these cytokines by about 45%. To study the mechanism, we examined the role of oxidative stress. ML decreased the amount of lipid peroxides by 43% and the expression of NADPH oxidase subunits in WAT, which was consistent with the results of TNF-α and MCP-1. Thus our results indicate that ML ameliorates adipocytokine dysregulation by inhibiting oxidative stress in WAT of obese mice, and that ML may have a potential for the treatment of the metabolic syndrome as well as reducing adverse effects of Pio.


F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 2515 ◽  
Author(s):  
Marleen M. J. van Greevenbroek ◽  
Casper G. Schalkwijk ◽  
Coen D.A. Stehouwer

The ongoing worldwide obesity epidemic makes the metabolic syndrome an increasingly important entity. In this review, we provide a short background on the metabolic syndrome, we discuss recent developments in the three main options that have been identified for intervention in the metabolic syndrome, i.e. lifestyle and surgical and pharmacological interventions, and we focus on different views in the literature and also include our own viewpoints on the metabolic syndrome. In addition, we discuss some emerging treatment targets for adipose tissue dysfunction and low-grade inflammation, i.e. activation of the inflammasome and the complement system, and consider some selected opportunities for intervention in these processes.


Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 594
Author(s):  
Shima Taherkhani ◽  
Katsuhiko Suzuki ◽  
Ruheea Taskin Ruhee

One of the leading causes of obesity associated with oxidative stress (OS) is excessive consumption of nutrients, especially fast-foods, and a sedentary lifestyle, characterized by the ample accumulation of lipid in adipose tissue (AT). When the body needs energy, the lipid is broken down into glycerol (G) and free fatty acids (FFA) during the lipolysis process and transferred to various tissues in the body. Materials secreted from AT, especially adipocytokines (interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α)) and reactive oxygen species (ROS), are impressive in causing inflammation and OS of AT. There are several ways to improve obesity, but researchers have highly regarded the use of antioxidant supplements due to their neutralizing properties in removing ROS. In this review, we have examined the AT response to OS to antioxidant supplements focusing on animal studies. The results are inconsistent due to differences in the study duration and diversity in animals (strain, age, and sex). Therefore, there is a need for different studies, especially in humans.


Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 406
Author(s):  
Ernesto Martínez-Martínez ◽  
Francisco Souza-Neto ◽  
Sara Jiménez-González ◽  
Victoria Cachofeiro

The vascular system plays a central role in the transport of cells, oxygen and nutrients between different regions of the body, depending on the needs, as well as of metabolic waste products for their elimination. While the structure of different components of the vascular system varies, these structures, especially those of main arteries and arterioles, can be affected by the presence of different cardiovascular risk factors, including obesity. This vascular remodeling is mainly characterized by a thickening of the media layer as a consequence of changes in smooth muscle cells or excessive fibrosis accumulation. These vascular changes associated with obesity can trigger functional alterations, with endothelial dysfunction and vascular stiffness being especially common features of obese vessels. These changes can also lead to impaired tissue perfusion that may affect multiple tissues and organs. In this review, we focus on the role played by perivascular adipose tissue, the activation of the renin-angiotensin-aldosterone system and endoplasmic reticulum stress in the vascular dysfunction associated with obesity. In addition, the participation of oxidative stress in this vascular damage, which can be produced in the perivascular adipose tissue as well as in other components of the vascular wall, is updated.


Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1233
Author(s):  
Fátima O. Martins ◽  
Joana F. Sacramento ◽  
Elena Olea ◽  
Bernardete F. Melo ◽  
Jesus Prieto-Lloret ◽  
...  

Several studies demonstrated a link between obstructive sleep apnea (OSA) and the development of insulin resistance. However, the main event triggering insulin resistance in OSA remains to be clarified. Herein, we investigated the effect of mild and severe chronic intermittent hypoxia (CIH) on whole-body metabolic deregulation and visceral adipose tissue dysfunction. Moreover, we studied the contribution of obesity to CIH-induced dysmetabolic states. Experiments were performed in male Wistar rats submitted to a control and high-fat (HF) diet. Two CIH protocols were tested: A mild CIH paradigm (5/6 hypoxic (5% O2) cycles/h, 10.5 h/day) during 35 days and a severe CIH paradigm (30 hypoxic (5% O2) cycles, 8 h/day) during 15 days. Fasting glycemia, insulinemia, insulin sensitivity, weight, and fat mass were assessed. Adipose tissue hypoxia, inflammation, angiogenesis, oxidative stress, and metabolism were investigated. Mild and severe CIH increased insulin levels and induced whole-body insulin resistance in control animals, effects not associated with weight gain. In control animals, CIH did not modify adipocytes perimeter as well as adipose tissue hypoxia, angiogenesis, inflammation or oxidative stress. In HF animals, severe CIH attenuated the increase in adipocytes perimeter, adipose tissue hypoxia, angiogenesis, and dysmetabolism. In conclusion, adipose tissue dysfunction is not the main trigger for initial dysmetabolism in CIH. CIH in an early stage might have a protective role against the deleterious effects of HF diet on adipose tissue metabolism.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Yahya M. Naguib ◽  
Rehab M. Samaka ◽  
Mohamed S. Rizk ◽  
Omnia Ameen ◽  
Shaimaa M. Motawea

Abstract Background The prevalence of hypertension and obesity has increased significantly in recent decades. Hypertension and obesity often coexist, and both are associated with increased cardiovascular mortality. Obese hypertensive patients usually require special anti-hypertensive treatment strategy due to the increased risk of treatment resistance. Molecules that can target both obesity and hypertension underlying pathologies should get more attention. Herein, we evaluated the therapeutic effects of telmisartan, with special interest in visceral adipose tissue dysfunction, in obesity-related hypertension rat model. Methods Thirty male Wistar rats weighing 150–200 g were equally divided into: 1—Control group (fed normal laboratory diet for 24 weeks), 2—Diet-induced obesity group (DIO, fed high fat diet for 24 weeks), and 3—Diet-induced obesity treated with telmisartan group (DIO + Tel, fed high fat diet and received telmisartan for 24 weeks). At the end of the study, anthropometrical parameters were evaluated. Systolic blood pressure and heart rate were measured. Blood samples were collected for the measurement of serum lipids, adipokines, cardiac, renal, inflammatory, and oxidative stress biomarkers. Kidneys were removed and used for histopathological studies, and visceral adipose tissue was utilized for histopathological, immunohistochemical and RT-PCR studies. Results High fat diet resulted in obesity-related changes in anthropometrical parameters, elevation of blood pressure, increase in heart rate, higher serum levels of cardiac, inflammatory and kidney function biomarkers, with altered serum lipids, adipokines and oxidative stress markers. Morphological changes (H&E and PAS-stained sections) were noticed in kidneys and visceral adipose tissue. Immunohistochemistry and RT-PCR studies confirmed adipose tissue dysfunction and over-expression of inflammatory and oxidative stress proteins. Telmisartan countered obesity-induced alterations in cardiovascular, renal, and adipose tissue functions. Conclusion Adipose tissue dysfunction could be the core pathophysiology of obesity-related hypertension. Besides its anti-hypertensive effect, telmisartan had profound actions on visceral adipose tissue structure and function. Attention should be given to polymodal molecules targeting adipose tissue-related disorders.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1669-1669
Author(s):  
Ya Pei ◽  
Hye Won Kang

Abstract Objectives Under obesity state, adipose tissue derived inflammatory mediators circulate all over the body and induce low-grade chronic inflammation, which is the main cause for the development of metabolic diseases. Moreover, inflammation-induced reactive oxygen species (ROS) cause oxidative stress, a process in damaging cellular structure and functions. Recently, microRNAs (miRNAs) were found to potentially regulate inflammation and its associated diseases. Brown adipose tissue (BAT) protects against obesity through thermogenic activity to increase energy expenditure. However, high levels of inflammation, ROS generation and aberrant level of miRNAs result in the dysfunction of BAT. Previously, quercetin showed anti-obesity effect through BAT activation. Thus, the purpose of this study was sought to investigate the effect of quercetin on high fat diet (HFD)-induced inflammation and oxidative stress in BAT. Methods C57BL/6 male mice were fed with a HFD or HFD supplemented with 1% quercetin (HFDQ) for 16 weeks. Total RNA was isolated from BAT to measure the expression of target mRNAs such as tumor necrosis factor alpha (TNFa), interleukin (IL) 1b, IL6, inducible nitric oxide synthase (iNOS), cyclooxygenase (COX) 2, NADPH oxidase (NOX) 2, nuclear factor E2-related factor (NRF) 2, superoxide dismutase (SOD) 2, SOD3, and catalase that are involved in regulation of inflammation and oxidative stress, and microRNA (miRNA)-155, a master regulator of inflammation, using a quantitative PCR. Results BAT of HFDQ-fed mice exhibited decreased expression of COX2, TNFa, IL1b, IL6, and iNOS compared to that of HFD-induced obese mice. NOX2 gene encoding an enzyme that generates ROS was also decreased in BAT of HFDQ-fed mice. The genes such as SOD2, SOD3, NRF2, and catalase that are involved in regulation of antioxidant enzymes were significantly increased. As the cognate gene of TNFa, miRNA-155 levels were downregulated. Conclusions Quercetin ameliorates HFD-induced inflammation and oxidative stress in BAT by regulating miRNA-155. Intake of quercetin may improve obese conditions by regulating BAT function through anti-inflammatory and antioxidant effects. Funding Sources This work was supported by USDA.


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