scholarly journals Impact of Dietary Restriction Regimens on Mitochondria, Heart, and Endothelial Function: A Brief Overview

2021 ◽  
Vol 12 ◽  
Author(s):  
Cristina Elena Savencu ◽  
Adina Linţa ◽  
Gianina Farcaş ◽  
Anca Mihaela Bînă ◽  
Octavian Marius Creţu ◽  
...  

Caloric restriction (CR) and intermittent fasting (IF) are strategies aimed to promote health beneficial effects by interfering with several mechanisms responsible for cardiovascular diseases. Both dietary approaches decrease body weight, insulin resistance, blood pressure, lipids, and inflammatory status. All these favorable effects are the result of several metabolic adjustments, which have been addressed in this review, i.e., the improvement of mitochondrial biogenesis, the reduction of reactive oxygen species (ROS) production, and the improvement of cardiac and vascular function. CR and IF are able to modulate mitochondrial function via interference with dynamics (i.e., fusion and fission), respiration, and related oxidative stress. In the cardiovascular system, both dietary interventions are able to improve endothelium-dependent relaxation, reduce cardiac hypertrophy, and activate antiapoptotic signaling cascades. Further clinical studies are required to assess the long-term safety in the clinical setting.

Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2475
Author(s):  
Sanne Ahles ◽  
Yala R. Stevens ◽  
Peter J. Joris ◽  
David Vauzour ◽  
Jos Adam ◽  
...  

Cognitive decline is associated with lifestyle-related factors such as overweight, blood pressure, and dietary composition. Studies have reported beneficial effects of dietary anthocyanins on cognition in older adults and children. However, the effect of anthocyanin-rich Aronia melanocarpa extract (AME) on cognition is unknown. Therefore, this study aimed to determine the effect of long-term supplementation with AME on cognitive performance, mood, and vascular function in healthy, middle-aged, overweight adults. In a randomized double-blind placebo-controlled parallel study, 101 participants either consumed 90 mg AME, 150 mg AME, or placebo for 24 weeks. The grooved pegboard test, number cross-out test, and Stroop test were performed as measures for psychomotor speed, attention, and cognitive flexibility. Mood was evaluated with a visual analogue scale, serum brain-derived neurotrophic factor (BDNF) was determined, and vascular function was assessed by carotid ultrasounds and blood pressure measurements. AME improved psychomotor speed compared to placebo (90 mg AME: change = −3.37; p = 0.009). Furthermore, 150 mg AME decreased brachial diastolic blood pressure compared to 90 mg AME (change = 2.44; p = 0.011), but not compared to placebo. Attention, cognitive flexibility, BDNF, and other vascular parameters were not affected. In conclusion, AME supplementation showed an indication of beneficial effects on cognitive performance and blood pressure in individuals at risk of cognitive decline.


2015 ◽  
Vol 6 (2) ◽  
pp. 105-117 ◽  
Author(s):  
Giusi Taormina ◽  
Mario G. Mirisola

AbstractMany aging theories and their related molecular mechanisms have been proposed. Simple model organisms such as yeasts, worms, fruit flies and others have massively contributed to their clarification, and many genes and pathways have been associated with longevity regulation. Among them, insulin/IGF-1 plays a key and evolutionary conserved role. Interestingly, dietary interventions can modulate this pathway. Calorie restriction (CR), intermittent fasting, and protein and amino acid restriction prolong the lifespan of mammals by IGF-1 regulation. However, some recent findings support the hypothesis that the long-term effects of diet also involve epigenetic mechanisms. In this review, we describe the best characterized aging pathways and highlight the role of epigenetics in diet-mediated longevity.


Author(s):  
Ana María Briones ◽  
Raquel Rodrigues-Díez

Mineralocorticoid receptor (MR) and its main ligand aldosterone, play a key role in the regulation of blood pressure through their effects increasing sodium and water reabsorption. MR antagonists are effective drugs that are currently used in selected patients with resistant hypertension. In addition, these drugs increase patients survival in specific circumstances such as heart failure, they offer renal protection in chronic kidney disease patients and they have beneficial effects in other pathologies. Besides MR cardiorenal effects, it is now accepted that MR is expressed in other tissues and cells such as vascular smooth muscle cells and endothelial cells where excessive MR activation induces deleterious effects such as vascular remodeling and stiffness and endothelial dysfunction, which are prognostic factors for future cardiovascular events. Moreover, novel evidence demonstrate that MR is also expressed in non-vascular cells adjacent to vessels such as immune cells and adipocytes that might influence vascular function and structure. Among the mechanisms responsible for these effects of MR are genomic and non genomic mechanisms that facilitate reactive oxygen species production mainly from the NADPH oxidase enzyme, as well as production of other inflammatory mediators. Here we review the experimental and clinical evidence that suggest that MR activation by aldosterone is an important mediator of vascular damage through the production of reactive oxygen species.


Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 216
Author(s):  
Simone Patergnani ◽  
Esmaa Bouhamida ◽  
Sara Leo ◽  
Paolo Pinton ◽  
Alessandro Rimessi

A decline in mitochondrial redox homeostasis has been associated with the development of a wide range of inflammatory-related diseases. Continue discoveries demonstrate that mitochondria are pivotal elements to trigger inflammation and stimulate innate immune signaling cascades to intensify the inflammatory response at front of different stimuli. Here, we review the evidence that an exacerbation in the levels of mitochondrial-derived reactive oxygen species (ROS) contribute to mito-inflammation, a new concept that identifies the compartmentalization of the inflammatory process, in which the mitochondrion acts as central regulator, checkpoint, and arbitrator. In particular, we discuss how ROS contribute to specific aspects of mito-inflammation in different inflammatory-related diseases, such as neurodegenerative disorders, cancer, pulmonary diseases, diabetes, and cardiovascular diseases. Taken together, these observations indicate that mitochondrial ROS influence and regulate a number of key aspects of mito-inflammation and that strategies directed to reduce or neutralize mitochondrial ROS levels might have broad beneficial effects on inflammatory-related diseases.


Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 3179
Author(s):  
María Morales-Suarez-Varela ◽  
Ester Collado Sánchez ◽  
Isabel Peraita-Costa ◽  
Agustín Llopis-Morales ◽  
José M. Soriano

Intermittent fasting has become popular in recent years and is controversially presented as a possible therapeutic adjunct. A bibliographic review of the literature on intermittent fasting and obesity, diabetes, and multiple sclerosis was carried out. The scientific quality of the methodology and the results obtained were evaluated in pairs. Intermittent fasting has beneficial effects on the lipid profile, and it is associated with weight loss and a modification of the distribution of abdominal fat in people with obesity and type 2 diabetes as well as an improvement in the control of glycemic levels. In patients with multiple sclerosis, the data available are too scarce to draw any firm conclusions, but it does appear that intermittent fasting may be a safe and feasible intervention. However, it is necessary to continue investigating its long-term effects since so far, the studies carried out are small and of short duration.


2018 ◽  
Vol 96 (3) ◽  
pp. 232-240
Author(s):  
Leonardo Souza-Silva ◽  
Rheure Alves-Lopes ◽  
Jéssica Silva Miguez ◽  
Vanessa Dela Justina ◽  
Karla Bianca Neves ◽  
...  

Overproduction of superoxide anion (•O2−) and O-linked β-N-acetylglucosamine (O-GlcNAc) modification in the vascular system are contributors to endothelial dysfunction. This study tested the hypothesis that increased levels of O-GlcNAc-modified proteins contribute to •O2− production via activation of NADPH oxidase, resulting in impaired vasodilation. Rat aortic segments and vascular smooth muscle cells (VSMCs) were incubated with vehicle (methanol) or O-(2-acetamido-2-deoxy-d-glucopyranosylidenamino) N-phenylcarbamate (PUGNAc) (100 μM). PUGNAc produced a time-dependent increase in O-GlcNAc levels in VSMC and decreased endothelium-dependent relaxation, which was prevented by apocynin and tiron, suggesting that •O2− contributes to endothelial dysfunction under augmented O-GlcNAc levels. Aortic segments incubated with PUGNAc also exhibited increased levels of reactive oxygen species, assessed by dihydroethidium fluorescence, and augmented •O2− production, determined by lucigenin-enhanced chemiluminescence. Additionally, PUGNAc treatment increased Nox-1 and Nox-4 protein expression in aortas and VSMCs. Translocation of the p47phox subunit from the cytosol to the membrane was greater in aortas incubated with PUGNAc. VSMCs displayed increased p22phox protein expression after PUGNAc incubation, suggesting that NADPH oxidase is activated in conditions where O-GlcNAc protein levels are increased. In conclusion, O-GlcNAc levels reduce endothelium-dependent relaxation by overproduction of •O2− via activation of NADPH oxidase. This may represent an additional mechanism by which augmented O-GlcNAc levels impair vascular function.


2021 ◽  
Vol 12 ◽  
Author(s):  
Yan Pan ◽  
Shuo Sun ◽  
Xingxing Wang ◽  
Aidong Chen ◽  
Xuejie Fei ◽  
...  

PurposeSalusin-β, a multifunctional vasoactive peptide, has a potentially important function in the pathological development of hypertension. However, the exact functional role of salusin-β and the underlying mechanism in this process are still not fully understood. The current study aimed to investigate the effects of silencing salusin-β on vascular function and vascular remodeling, as well as its signaling pathways in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY).MethodsSilencing salusin-β was performed by caudal vein injection of adenovirus expressing salusin-β short hairpin RNA (shRNA). Acetylcholine (ACh)-induced endothelium-dependent relaxation was used to evaluate vasodilator function, and high K+ solution-induced constriction was used to evaluate vasoconstriction function.ResultsSalusin-β levels in plasma and its protein expression in mesenteric artery (MA), coronary artery (CA), and pulmonary artery (PA) of SHR were higher than those in WKY. The salusin-β level and expression were decreased effectively by salusin-β shRNA. Knockdown of salusin-β decreased arterial blood pressure (ABP) and high K+ solution-induced vascular constrictions, and improved the endothelium-dependent relaxation and vascular remodeling in SHR. The improved effect of silencing salusin-β on ACh-induced relaxation in SHR was almost blocked by the nitric oxide synthase (NOS) inhibitor L-NAME. Compared to WKY, the endothelial NOS (eNOS) activity and level, and nitric oxide (NO) level were decreased, while NAD(P)H oxidase activity and reactive oxygen species (ROS) levels in MA, CA, and PA of SHR were increased, which were all redressed by salusin-β knockdown.ConclusionThese results indicate that knockdown of salusin-β improves endothelium-dependent vascular relaxation and vascular remodeling and decreases ABP and vasoconstriction in SHR, which might be accomplished by increasing eNOS activation and NO release while inhibiting NAD(P)H oxidase derived-ROS generation. Scavenging salusin-β improves vascular function and then prevents the development and progression of vasculopathy of hypertension.


2020 ◽  
Author(s):  
Lynda Grine ◽  
Niels Hilhorst ◽  
Nathalie Michels ◽  
Souheila Abbedou ◽  
Stefaan De Henauw ◽  
...  

BACKGROUND Psoriasis is a complex disease associated with multiple comorbidities, including metabolic syndrome and leaky gut syndrome. Dietary lifestyle interventions have been reported to affect the disease in terms of lesional severity. It remains unclear how diets affect these comorbidities and the general health in psoriasis patients. Modified Intermittent Fasting (MIF) on 2 non-consecutive days has shown beneficial effects on metabolic parameters. A significant advantage of MIF over the currently investigated dietary changes is its feasibility. OBJECTIVE Here, we aim to study the effects of MIF on skin, gut and metabolic health in psoriasis patients. METHODS A two-arm pilot prospective cross-over randomized control trial (RCT) will be performed in 20 patients with psoriasis as a pilot study. Patients will be randomized 1:1 to either start with MIF and subsequent regular diet for 12 weeks each or to start with regular diet and subsequent MIF for 12 weeks each. The following parameters will be assessed: demographics, disease phenotype, medical and familial history, psoriasis severity, dermatology-specific and general quality of life, nutritional and physical habits, mental and intestinal health, intestinal and cutaneous integrity, inflammatory and metabolic markers, and satisfaction. RESULTS The aim is to uncover the effects of MIF on psoriasis severity and gut health integrity through clinical and molecular investigation. More precisely, we want to map the evolution of the different markers in response to MIF as compared to the regular diet, such as psoriasis severity, permeability and inflammation. CONCLUSIONS Understanding how dietary lifestyles can affect epithelial lineages such as the skin and gut, will greatly improve our understanding on the development of psoriasis and may pose a non-pharmacological venue for treatments. CLINICALTRIAL ClinicalTrials.gov, NCT04418791. Registered June 5 2020, https://clinicaltrials.gov/ct2/show/NCT04418791. Current protocol date/version: May 20 2020


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1231-1231
Author(s):  
Giulio Pasinetti

Abstract Objectives Chronic stress activates danger-associated molecular patterns (DAMPs), stimulating the NLRP3 inflammasome. NLRP3 activation triggers the release of pro-inflammatory cytokine IL-1β. The activity of the NLRP3 inflammasome propagates pro-inflammatory signaling cascades implicated in the onset of depression. Our previous studies show that polyphenolic compounds were found to ameliorate stress induced depression in mouse models. However, the relevant mechanism has not been identified. This study examined the effect of administering polyphenols on DAMP signaling in enriched mice microglia. Methods This study examined the effect of administering polyphenols on DAMP signaling in mice microglia. To recapitulate stress-induced depression, mice underwent chronic unpredictable stress (CUS). Microglia were isolated at various time points throughout the CUS protocol. We also assessed long-term persistent changes after CUS and susceptibility to subthreshold unpredictable stress (US) re-exposure. Results Interestingly, the development of US – induced depression and anxiety depended upon a previous exposure to CUS. We found that CUS caused robust upregulation of IL-1β mRNA in enriched microglia, an effect that persists for up to 4 weeks following CUS exposure. Following the subthreshold US re-exposure, we observed the upregulation of pro- IL-1β as well as pro-receptor for advanced glycation end products (RAGE). Toll-like receptor 4 (TLR-4) was not. We also observed an increase in RAGE mRNA expression when mice were exposed to US prior to the start of the CUS paradigm. Importantly, a primary exposure to US, was sufficient to increase RAGE mRNA expression. We found that polyphenol administration significantly improved CUS-induced depressive-like phenotypes and also reversed neuroinflammation in mice. Treatment with dietary flavonoids prevented upregulation of IL-1β, RAGE mRNA, which reflects the ability of polyphenols that may have begun following the primary exposure to US. Conclusions Taken all together, the results provide evidence of the role of dietary polyphenols in preventing persistent microglial activation, which has been shown to result in reduced long term vulnerability to depressive-like behaviors following expose to chronic stress. Funding Sources This study was supported by a P50 CARBON Center grant from the NCCIH/ODS.


2021 ◽  
Vol 13 (11) ◽  
pp. 2131
Author(s):  
Jamon Van Den Hoek ◽  
Alexander C. Smith ◽  
Kaspar Hurni ◽  
Sumeet Saksena ◽  
Jefferson Fox

Accurate remote sensing of mountainous forest cover change is important for myriad social and ecological reasons, but is challenged by topographic and illumination conditions that can affect detection of forests. Several topographic illumination correction (TIC) approaches have been developed to mitigate these effects, but existing research has focused mostly on whether TIC improves forest cover classification accuracy and has usually found only marginal gains. However, the beneficial effects of TIC may go well beyond accuracy since TIC promises to improve detection of low illuminated forest cover and thereby normalize measurements of the amount, geographic distribution, and rate of forest cover change regardless of illumination. To assess the effects of TIC on the extent and geographic distribution of forest cover change, in addition to classification accuracy, we mapped forest cover across mountainous Nepal using a 25-year (1992–2016) gap-filled Landsat time series in two ways—with and without TIC (i.e., nonTIC)—and classified annual forest cover using a Random Forest classifier. We found that TIC modestly increased classifier accuracy and produced more conservative estimates of net forest cover change across Nepal (−5.2% from 1992–2016) TIC. TIC also resulted in a more even distribution of forest cover gain across Nepal with 3–5% more net gain and 4–6% more regenerated forest in the least illuminated regions. These results show that TIC helped to normalize forest cover change across varying illumination conditions with particular benefits for detecting mountainous forest cover gain. We encourage the use of TIC for satellite remote sensing detection of long-term mountainous forest cover change.


Sign in / Sign up

Export Citation Format

Share Document