scholarly journals Targeting mitochondrial biogenesis: a potential approach for preventing and controlling diabetes

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Ritika Singh ◽  
Lucy Mohapatra ◽  
Alok Shiomurthi Tripathi
Keyword(s):  
Insulin Resistance ◽  
Reactive Oxygen Species ◽  
Mitochondrial Biogenesis ◽  
Diabetic Complications ◽  
Reactive Oxygen ◽  
Main Body ◽  
Oxygen Species ◽  
Treatment And Prevention ◽  
Skeletal Muscle Insulin Resistance ◽  
Mitochondrial Number

Abstract Background Diabetes mellitus is a lingering hyperglycemic ailment resulting in several life-threatening difficulties. Enduring hyperglycemia often persuades the buildup of reactive oxygen species that are the significant pathological makers of diabetic complications. The mitochondrial dysfunction, with mitochondrial damage and too much production of reactive oxygen species, have been proposed to be convoluted in the progress of insulin resistance. Numerous studies advocate that agents that enhance the mitochondrial number and/or decrease their dysfunction, could be greatly helpful in management of diabetes and its complications. Main body Mitochondrial biogenesis is an extremely delimited procedure arbitrated by numerous transcription influences, in which mitochondrial fusion and fission happen in synchronization in a standard vigorous cell. But this synchronization is greatly disturbed in diabetic condition designated by modification in the working of several important transcription factors regulating the expressions of different genes. Numerous preclinical and clinical investigations have suggested that, the compromised functions of mitochondria play a significant protagonist in development of pancreatic β-cell dysfunction, skeletal muscle insulin resistance and several diabetic complications. However, there are several phytoconstituents performing through numerous alleyways, either unswervingly by motivating biogenesis or indirectly by constraining or averting dysfunction and producing a beneficial effect on overall function of the mitochondria. Conclusion This review describes standard mitochondrial physiology and anomalous modifications that transpire in answer to persistent hyperglycemia in diabetes condition. It also discusses about the different phytoconstituents that can affect the biogenesis pathways of mitochondria and thus can be used in the treatment and prevention of diabetes.

The Role of Reactive Oxygen Species in Tumor Treatment and its Impact on Bone Marrow Hematopoiesis

2020 ◽  
Vol 21 (5) ◽  
pp. 477-498
Author(s):  
Yongfeng Chen ◽  
Xingjing Luo ◽  
Zhenyou Zou ◽  
Yong Liang
Keyword(s):  
Reactive Oxygen Species ◽  
Bone Marrow ◽  
Oxidative Damage ◽  
Tumor Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tumor Treatment ◽  
Normal Cells ◽  
Treatment And Prevention

Reactive oxygen species (ROS), an important molecule inducing oxidative stress in organisms, play a key role in tumorigenesis, tumor progression and recurrence. Recent findings on ROS have shown that ROS can be used to treat cancer as they accelerate the death of tumor cells. At present, pro-oxidant drugs that are intended to increase ROS levels of the tumor cells have been widely used in the clinic. However, ROS are a double-edged sword in the treatment of tumors. High levels of ROS induce not only the death of tumor cells but also oxidative damage to normal cells, especially bone marrow hemopoietic cells, which leads to bone marrow suppression and (or) other side effects, weak efficacy of tumor treatment and even threatening patients’ life. How to enhance the killing effect of ROS on tumor cells while avoiding oxidative damage to the normal cells has become an urgent issue. This study is a review of the latest progress in the role of ROS-mediated programmed death in tumor treatment and prevention and treatment of oxidative damage in bone marrow induced by ROS.

scholarly journals Fanconi Anemia Links Reactive Oxygen Species to Insulin Resistance and Obesity

2012 ◽  
Vol 17 (8) ◽  
pp. 1083-1098 ◽  
Author(s):  
Jie Li ◽  
Jared Sipple ◽  
Suzette Maynard ◽  
Parinda A. Mehta ◽  
Susan R. Rose ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Reactive Oxygen Species ◽  
Fanconi Anemia ◽  
Reactive Oxygen ◽  
Oxygen Species

Endothelium-specific insulin resistance leads to accelerated atherosclerosis in areas with disturbed flow patterns: A role for reactive oxygen species

2013 ◽  
Vol 230 (1) ◽  
pp. 131-139 ◽  
Author(s):  
Matthew C. Gage ◽  
Nadira Y. Yuldasheva ◽  
Hema Viswambharan ◽  
Piruthivi Sukumar ◽  
Richard M. Cubbon ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Flow Patterns ◽  
Oxygen Species ◽  
Disturbed Flow ◽  
Accelerated Atherosclerosis ◽  
Specific Insulin

129 EFFECT OF SERUM SUPPLEMENTATION ON AMP-ACTIVATED PROTEIN KINASE (AMPK) ACTIVITY AND LIPID METABOLISM OF IN VITRO-CULTURED BOVINE EMBRYOS

2015 ◽  
Vol 27 (1) ◽  
pp. 156
Author(s):  
S. Prastowo ◽  
F. Rings ◽  
D. S. Wondim ◽  
E. Tholen ◽  
C. Looft ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Mitochondrial Biogenesis ◽  
Reactive Oxygen ◽  
Rna Isolation ◽  
Mitochondrial Activity ◽  
Oxygen Species ◽  
Bovine Embryos ◽  
Fluorescent Intensity ◽  
Ampk Activity

A major problem of embryos cultured in vitro with serum is cytoplasmic lipid accumulation resulting in lower cryotolerance compared with those derived from in vivo or in the absence of serum. AMPK is known as a master regulator of lipid, glucose, and protein metabolism in mammalian cells. Moreover, it has been reported as controller of acetyl-CoA carboxylase α (ACC), the gene responsible for lipid synthesis, and associated with mitochondrial biogenesis and activities in response to oxidative stress. In the present study we aimed to investigate the regulation of AMPK during serum supplementation in vitro. For this, bovine embryos were produced in vitro in SOF media supplemented with oestrous cow serum or fatty acid–free BSA as a system without serum. Triplicate pools (each 10 blastocysts) from each group were used for RNA isolation using Arcturus®PicoPure®RNA Isolation Kit (Life Technologies, USA). Reverse transcription was performed using a combination of Oligo(dT)23 and random primers. Quantification of AMPK catalytic α1 (AMPKA1), ACC, peroxisome proliferator-activated receptor gamma coactivator 1 α (PGC1A), and sterol regulatory element binding transcription factor 2 (SREBP2) transcripts were performed using ABI PRISM® 7000 SDS system (Applied Biosystems, Foster City, CA, USA) using GAPDH as internal control. Normalized log-transformed transcript amount data were statistically analysed using t-test. In addition, AMPK protein was detected by immunofluorescence, mitochondrial activity by MitoTracker® Red (Invitrogen, Carlsbad, CA, USA), and reactive oxygen species by H2DCFDA molecular probe (Life Technologies, USA), and fluorescent intensity signals were visualised under confocal laser scanning microscopy LSM 710 (Carl Zeiss, Germany). Results showed that the expression of AMPKA1, PGC1A, a mitochondrial biogenesis protein, and SREBP2, a regulator of lipid oxidation, were found to be lower (0.4-, 0.2-, and 0.7-fold, respectively; P < 0.05) in blastocysts derived from cultured with serum compared to without serum. By contrast, ACC was up-regulated in blastocysts cultured with serum by 1.8-fold (P < 0.05) compared to without serum. In comparison to blastocyst cultured without serum, a reduced fluorescent intensity was observed in AMPKA1 protein and mitochondrial activity in blastocyst cultured with serum. The presence of serum was also found to be involved in increasing reactive oxygen species accumulation in embryos cultured with serum. The reduced level of AMPK leads to increased ACC and subsequently enhanced conversion of fatty acids into lipid, which is associated with reduced mitochondrial biogenesis protein, elevated reactive oxygen species level, and reduced lipid oxidation by suppression of SREBP2. In conclusion, the presence of serum in in vitro culture environment affected the AMPK activity and thereby genes associated with lipid metabolism in early bovine embryos.

scholarly journals Aldosterone Inhibits Insulin-Induced Glucose Uptake by Degradation of Insulin Receptor Substrate (IRS) 1 and IRS2 via a Reactive Oxygen Species-Mediated Pathway in 3T3-L1 Adipocytes

Endocrinology ◽  
2008 ◽  
Vol 150 (4) ◽  
pp. 1662-1669 ◽  
Author(s):  
Tsutomu Wada ◽  
Satoshi Ohshima ◽  
Eriko Fujisawa ◽  
Daisuke Koya ◽  
Hiroshi Tsuneki ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Reactive Oxygen Species ◽  
Glucocorticoid Receptor ◽  
Insulin Receptor ◽  
Receptor Antagonist ◽  
Glucose Uptake ◽  
Reactive Oxygen ◽  
Insulin Receptor Substrate ◽  
Oxygen Species ◽  
Metabolic Signaling

Serum aldosterone level is clinically known to correlate with body weight and insulin resistance. Because the underlying molecular mechanism is largely unknown, we examined the effect of aldosterone on insulin-induced metabolic signaling leading to glucose uptake in 3T3-L1 adipocytes. Aldosterone reduced the amounts of insulin receptor substrate (IRS) 1 and IRS2 in a time- and dose-dependent manner. As a result, insulin-induced phosphorylation of Akt-1 and -2, and subsequent uptake of 2-deoxyglucose were decreased. Degradation of IRSs was effectively prevented by a glucocorticoid receptor antagonist and antioxidant N-acetylcysteine, but not by a mineralocorticoid receptor antagonist. Because aldosterone induced phosphorylation of IRS1 at Ser307, responsible kinases were investigated, and we revealed that rapamycin and BMS345541, but neither SP600125 nor calphostin C, conferred for degradation of IRSs. Although lactacystin prevented the degradation of IRSs, glucose uptake was not preserved. Importantly, sucrose-gradient-sediment intracellular fraction analysis revealed that lactacystin did not effectively restore the reduction of IRS1 in the low-density microsome fraction, important for the transduction of insulin’s metabolic signaling. These results indicate that aldosterone deteriorates metabolic action of insulin by facilitating the degradation of IRS1 and IRS2 via glucocorticoid receptor-mediated production of reactive oxygen species, and activation of IκB Kinase β and target of rapamycin complex 1. Thus, aldosterone appears to be a novel key factor in the development of insulin resistance in visceral obesity.

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