scholarly journals Pericardial Adipose Tissue–Derived Leptin Promotes Myocardial Apoptosis in High‐Fat Diet–Induced Obese Rats Through Janus Kinase 2/Reactive Oxygen Species/Na+/K+‐ATPase Signaling Pathway

2021 ◽  
Author(s):  
Ping Wang ◽  
Chaodi Luo ◽  
Danjun Zhu ◽  
Yan Song ◽  
Lifei Cao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Adipose Tissue ◽  
High Fat Diet ◽  
Reactive Oxygen ◽  
Janus Kinase ◽  
Oxygen Species ◽  
High Fat ◽  
Myocardial Apoptosis ◽  
Pericardial Adipose Tissue ◽  
Obese Rats

Background Pathophysiologic mechanisms underlying cardiac structural and functional changes in obesity are complex and linked to adipocytokines released from pericardial adipose tissue (PAT) and cardiomyocyte apoptosis. Although leptin is involved in various pathological conditions, its role in paracrine action of pericardial adipose tissue on myocardial apoptosis remains unknown. This study was designed to investigate the role of PAT‐derived leptin on myocardial apoptosis in high‐fat diet–induced obese rats. Methods and Results Hearts were isolated from lean or high‐fat diet–induced obese Wistar rats for myocardial remodeling studies. Obese rats had abnormal myocardial structure, diastolic dysfunction, greatly elevated cardiac apoptosis, enhanced cardiac fibrosis, and increased oxidative stress level. ELISA detected significantly higher than circulating leptin level in PAT of obese, but not lean, rats. Western blot and immunohistochemical analyses demonstrated increased leptin receptor density in obese hearts. H9c2 cardiomyoblasts, after being exposed to PAT‐conditioned medium of obese rats, exhibited pronounced reactive oxygen species–mediated apoptosis, which was partially reversed by leptin antagonist. Moreover, leptin derived from PAT of obese rats inhibited Na + /K + ‐ATPase activity of H9c2 cells through stimulating reactive oxygen species, thereby activating calcium‐dependent apoptosis. Pretreatment with specific inhibitors revealed that Janus kinase 2/signal transducer and activator of transcription 3 and phosphoinositide 3‐kinase/protein kinase B signaling pathways were involved in leptin‐induced myocardial apoptosis. Conclusions PAT‐derived leptin induces myocardial apoptosis in high‐fat diet–induced obese rats via activating Janus kinase 2/signal transducer and activator of transcription 3/reactive oxygen species signaling pathway and inhibiting its downstream Na + /K + ‐ATPase activity.

Effect of somatostatin analog on high-fat diet-induced metabolic syndrome: Involvement of reactive oxygen species

Peptides ◽  
2010 ◽  
Vol 31 (4) ◽  
pp. 625-629 ◽  
Author(s):  
Wu Li ◽  
Yong-Hui Shi ◽  
Rui-li Yang ◽  
Jue Cui ◽  
Ying Xiao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Metabolic Syndrome ◽  
High Fat Diet ◽  
Reactive Oxygen ◽  
Somatostatin Analog ◽  
Oxygen Species ◽  
High Fat

scholarly journals Single bulb garlic oil improves interleukin-6 via decreased reactive oxygen species (ROS) in high-fat diet male mice

2019 ◽  
Vol 38 (2) ◽  
pp. 100 ◽  
Author(s):  
Riza Rahayu Ilmawati ◽  
Abdul Gofur ◽  
Sri Rahayu Lestari
Keyword(s):  
Reactive Oxygen Species ◽  
Interleukin 6 ◽  
High Fat Diet ◽  
Antioxidant Properties ◽  
Reactive Oxygen ◽  
Optimum Dose ◽  
Oxygen Species ◽  
Male Mice ◽  
High Fat ◽  
Garlic Oil

Background<br />High-fat diet (HFD) is highly responsible for the development of excessive reactive oxygen species (ROS). ROS and low-density lipoprotein (LDL) then trigger macrophage activation to secrete interleukin-6 (IL-6). Single bulb garlic or in Indonesian called bawang lanang is traditional medicine that possesses strong antioxidant properties. This study aimed to evaluate the effect of single bulb garlic oil (SBGO) on ROS, IL-6, and lymphocyte density in HFD-fed male mice.<br /><br />Methods<br />This was an experimental study on 24 male mice randomly subdivided into 6 groups: one group was fed a normal diet, whereas the remaining five groups were fed HFD for 45 days and were then treated with single bulb garlic oil 0 mg/kg, simvastatin 26 mg/kg BW, single bulb garlic oil 12.5 mg/kg BW, 25 mg/kg BW, and 50 mg/kg BW respectively for the next 35 days. At the end of treatment, the mice were dissected for collection of (i) serum in order to measure ROS and IL-6 levels using ELISA, (ii) aortas to measure IL-6 expression using immunohistochemistry-fluorescence (IHC-F) and to obtain lymphocytes from bone marrow and spleen which were then counted using a light microscope.<br /><br />Results<br />Our results indicated that SBGO decreased the ROS level, IL-6 level, IL-6 expression, and lymphocyte density in HFD mice. SBGO 12.5 mg/kg BW is the optimum dose in our study to reduce inflammation in HFD male mice.<br /><br />Conclusion<br />SBGO is useful to reduce inflammation and improve antioxidant imbalance, thus might be a potential antiatherogenic agent.

scholarly journals Estradiol and NADPH oxidase crosstalk regulates responses to high fat feeding in female mice

2019 ◽  
Vol 244 (10) ◽  
pp. 834-845 ◽  
Author(s):  
Martin J Ronis ◽  
Michael L Blackburn ◽  
Kartik Shankar ◽  
Matthew Ferguson ◽  
Mario A Cleves ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Adipose Tissue ◽  
Nadph Oxidase ◽  
Tissue Injury ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Wild Type ◽  
High Fat ◽  
Reactive Oxygen Species Signaling ◽  
Genotype Effects

We previously demonstrated protection against high fat-induced obesity in female but not male p47phox−/− mice lacking NADPH oxidase NOX1/2 activity. To test the role of estradiol (E2)-NOX crosstalk in development of this sexually dimorphic phenotype, we fed diets containing 42% fat/0.5% cholesterol to intact and ovariectomized wild type female C57BL/6 mice and female p47phox−/− mice and to ovariectomized mice where the diet was supplemented with an 1 mg/kg 17β estradiol (E2) for 12 weeks from PND28. Weight gain, gonadal fat pad weight, serum leptin and adiponectin, and adipose tissue inflammation were greater in intact wild type vs. p47 mice ( P < 0.05). Genotype effects on body weight/fat mass were abolished after ovariectomized and restored in OVX + E2 mice ( P < 0.05). The mRNA of downstream PPARγ targets CD36, lipoprotein lipase, and leptin was higher in intact wild type vs. p47phox−/− mice mice ( P < 0.05). Likewise, intact high fat-fed wild type mice had higher expression of the cytokine Mcp1; the pyroptosis marker Nirp3 and matrix remodeling and fibrosis markers Mmp2, Col1A1, and Col6a3 mRNAs ( P < 0.05). These genotype effects were reversed and restored by ovariectomized and OVX + E2, respectively ( P < 0.05). These data suggest that triglyceride accumulation in adipose tissue and development of adipose tissue injury in response to feeding diets high in fat and cholesterol is regulated by the balance between NOX-dependent reactive oxygen species signaling and E2-signaling during development. Loss of estrogens post menopause may increase the risk of obesity and metabolic syndrome as the result disinhibition of reactive oxygen species signaling. Impact statement Estrogens are known to regulate body composition. In addition, reactive oxygen species (ROS) produced by the action of NADPH oxidase (NOX) enzymes have been linked to obesity development. We examined development of obesity and adipose tissue injury in response to feeding “Western” diets high in fat and cholesterol in intact, ovariectomized (OVX), and estrogen-replaced (OVX + E2) wild type and p47phox−/− female mice where NOX2 activity is inhibited. Weight gain, gonadal fat pad weight, and adipose tissue inflammation were greater in intact WT vs. p47phox−/− mice. Genotype effects on body weight/fat mass were abolished after OVX and restored in OVX + E2 mice. These data indicate adipose tissue responses to feeding the “Western” diet is regulated by negative cross-talk between NOX-dependent ROS signaling and E2-signaling during development. Loss of estrogens post menopause may increase the risk of obesity and metabolic syndrome as the result disinhibition of ROS signaling.

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