289-OR: Aerobic Exercise Counteracts Mitochondrial Dysfunction in the Insulin Resistant Brain

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 289-OR
Author(s):  
GREGORY RUEGSEGGER ◽  
PATRICK M. VANDERBOOM ◽  
SURENDRA DASARI ◽  
KATHERINE KLAUS ◽  
K. SREEKUMARAN NAIR
Keyword(s):  
Aerobic Exercise ◽  
Mitochondrial Dysfunction ◽  
Insulin Resistant

scholarly journals Aerobic Exercise Counteracts Mitochondrial Dysfunction In The Insulin Resistant Brain

2020 ◽  
Vol 52 (7S) ◽  
pp. 1061-1061
Author(s):  
Gregory N. Ruegsegger ◽  
Patrick M. Vanderboom ◽  
Surendra Dasari ◽  
Katherine A. Klaus ◽  
K Sree Nair
Keyword(s):  
Aerobic Exercise ◽  
Mitochondrial Dysfunction ◽  
Insulin Resistant

Hyperbaric oxygen therapy attenuates D-galactose-induced-age-related cardiac dysfunction through mitigating cardiac mitochondrial dysfunction in pre-diabetic rats

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
C Bo-Htay ◽  
T Shwe ◽  
S Palee ◽  
T Pattarasakulchai ◽  
K Shinlapawittayatorn ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
High Fat Diet ◽  
Diabetic Rats ◽  
Normal Diet ◽  
Lv Function ◽  
High Fat ◽  
Insulin Resistant ◽  
Lv Dysfunction ◽  
Age Related ◽  
Mitochondrial Functions

Abstract Background D-galactose (D-gal) induced ageing has been shown to exacerbate left ventricular (LV) dysfunction via worsening of apoptosis and mitochondrial dysfunction in the heart of obese rats. Hyperbaric oxygen therapy (HBOT) has been demonstrated to exert anti-inflammatory and anti-apoptotic effects in multiple neurological disorders. However, the cardioprotective effect of HBOT on inflammation, apoptosis, LV and mitochondrial functions in D-gal induced ageing rats in the presence of obese-insulin resistant condition has never been investigated. Purpose We sought to determine the effect of HBOT on inflammation, apoptosis, mitochondrial functions and LV function in pre-diabetic rats with D-gal induced ageing. We hypothesized that HBOT attenuates D-gal induced cardiac mitochondrial dysfunctions and reduces inflammation and apoptosis, leading to improved LV function in pre-diabetic rats. Methods Forty-eight male Wistar rats were fed with either normal diet or high-fat diet for 12 weeks. Then, rats were treated with either vehicle groups (0.9% NSS, subcutaneous injection (SC)) or D-gal groups (150 mg/kg/day, SC) for 8 weeks. At week 21, rats in each group were equally divided into 6 sub-groups: normal diet fed rats treated with vehicle (NDV) sham, normal diet fed rats treated with D-gal (NDDg) sham, high fat diet fed rats treated with D-gal (HFDg) sham, high fat diet fed rats treated with vehicle (HFV) + HBOT, NDDg + HBOT and HFDg + HBOT. Sham treated rats were given normal concentration of O2 (flow rate of 80 L/min, 1 ATA for 60 minutes), whereas HBOT treated rats were subjected to 100% O2 (flow rate of 250 L/min, 2 ATA for 60 minutes), given once daily for 2 weeks. Results Under obese-insulin resistant condition, D-gal-induced ageing aggravated LV dysfunction (Fig 1A) and impaired cardiac mitochondrial function, increased cardiac inflammatory and apoptotic markers (Fig 1B). HBOT markedly reduced cardiac TNF-α level and TUNEL positive apoptotic cells, and improved cardiac mitochondrial function as indicated by decreased mitochondrial ROS production, mitochondrial depolarization and mitochondrial swelling, resulting in the restoration of the normal LV function in HFV and NDDg rats, compared to sham NDDg rats. In addition, in HFDg treated rats, HBOT attenuated cardiac TNF-α level, TUNEL positive apoptotic cells and cardiac mitochondrial dysfunction, compared to sham HFDg rats, leading to improved cardiac function as indicated by increased %LV ejection fraction (LVEF) (Figure 1). Conclusion HBOT efficiently alleviates D-gal-induced-age-related LV dysfunction through mitigating inflammation, apoptosis and mitochondrial dysfunction in pre-diabetic rats. Figure 1 Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): 1. The National Science and Technology Development Agency Thailand, 2. Thailand Research Fund Grants

Chronic treatment with prebiotics, probiotics and synbiotics attenuated cardiac dysfunction by improving cardiac mitochondrial dysfunction in male obese insulin-resistant rats

2017 ◽  
Vol 57 (6) ◽  
pp. 2091-2104 ◽  
Author(s):  
Wannipa Tunapong ◽  
Nattayaporn Apaijai ◽  
Sakawdaurn Yasom ◽  
Pongpan Tanajak ◽  
Keerati Wanchai ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Cardiac Dysfunction ◽  
Chronic Treatment ◽  
Insulin Resistant

Azoramide improves mitochondrial dysfunction in palmitate-induced insulin resistant H9c2 cells

2019 ◽  
Vol 461 (1-2) ◽  
pp. 65-72 ◽  
Author(s):  
Esma Nur Okatan ◽  
Yusuf Olgar ◽  
Erkan Tuncay ◽  
Belma Turan
Keyword(s):  
Mitochondrial Dysfunction ◽  
H9c2 Cells ◽  
Insulin Resistant

Garlic extract attenuates brain mitochondrial dysfunction and cognitive deficit in obese-insulin resistant rats

2014 ◽  
Vol 39 (12) ◽  
pp. 1373-1379 ◽  
Author(s):  
Hiranya Pintana ◽  
Jirapas Sripetchwandee ◽  
Luerat Supakul ◽  
Nattayaporn Apaijai ◽  
Nipon Chattipakorn ◽  
...  
Keyword(s):  
Body Weight ◽  
Cognitive Function ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Visceral Fat ◽  
Cognitive Deficit ◽  
Garlic Extract ◽  
Insulin Resistant ◽  
Mitochondrial Functions ◽  
Brain Mitochondrial Function

Oxidative stress in the obese-insulin resistant condition has been shown to affect cognitive as well as brain mitochondrial functions. Garlic extract has exerted a potent antioxidant effect. However, the effects of garlic extract on the brain of obese-insulin resistant rats have never been investigated. We hypothesized that garlic extract improves cognitive function and brain mitochondrial function in obese-insulin resistant rats induced by long-term high-fat diet (HFD) consumption. Male Wistar rats were fed either normal diet or HFD for 16 weeks (n = 24/group). At week 12, rats in each dietary group received either vehicle or garlic extract (250 and 500 mg·kg–1·day–1) for 28 days. Learning and memory behaviors, metabolic parameters, and brain mitochondrial function were determined at the end of treatment. HFD led to increased body weight, visceral fat, plasma insulin, cholesterol, and malondialdehyde (MDA) levels, indicating the development of insulin resistance. Furthermore, HFD rats had cognitive deficit and brain mitochondrial dysfunction. HFD rats treated with both doses of garlic extract had decreased body weight, visceral fat, plasma cholesterol, and MDA levels. Garlic extract also improved cognitive function and brain mitochondrial function, which were impaired in obese-insulin resistant rats caused by HFD consumption.

ID: 83: PRODUCTION OF SOLUBLE RECEPTOR FOR ADVANCED GLYCATION END-PRODUCTS FOLLOWING ACUTE AEROBIC EXERCISE IS GENDER SPECIFIC

2016 ◽  
Vol 64 (4) ◽  
pp. 928.2-929
Author(s):  
ER Miranda ◽  
JT Mey ◽  
BK Blackburn ◽  
JM Haus ◽  
SS Farabi ◽  
...  
Keyword(s):  
Aerobic Exercise ◽  
Advanced Glycation End Products ◽  
Acute Exercise ◽  
Primary Objective ◽  
Advanced Glycation ◽  
Insulin Resistant ◽  
Soluble Rage ◽  
Downstream Effectors ◽  
Glycation End Products ◽  
End Products

The Receptor for Advanced Glycation End Products (RAGE) is a transmembrane receptor that initiates a self-propagating inflammatory cascade and has been implicated in the onset of complications involved with aging, diabetes and neuroinflammation. Soluble RAGE (sRAGE) inhibits this inflammatory signaling by competitively binding to RAGE ligands without stimulating downstream effectors. Evidence from our lab demonstrates chronic aerobic exercise increases the cleaved isoform of sRAGE (sRAGEc). However, the effects of acute aerobic exercise on sRAGEc production have not been comprehensively examined. Furthermore, recent data suggests that estrogen may play a role in exacerbating RAGE signaling and perturbing sRAGE production in diabetic women. Therefore, the primary objective of this study was to investigate changes in plasma sRAGE with acute aerobic exercise in both lean healthy (LH) and obese insulin resistant (OB-IR) individuals. A secondary objective of the study was to compare exercise responses between men and women. 8 LH participants (4 M, 4 F) and 14 OB-IR participants (4 M, 10 F) were recruited for the study. VO2max was determined via treadmill test and participants returned to the lab on a separate day following an overnight fast and exercised at 65% VO2max for 30 minutes. Blood samples were collected before and following exercise after participants rested in seated position for 30 minutes. Quantification of plasma sRAGE and endogeonous secretory RAGE were determined via ELISA and sRAGEc was calculated by subtraction. Between-group comparisons were made via independent T Test and the effect of gender was analyzed via two-way ANOVA. At baseline the OB-IR group was older (41±3 y vs. 26±1 y, p<.001), more obese (BMI 35.1±0.9 vs. 22.2±0.9 kg . m−2, p<.001) and less aerobically fit (VO2max 27.8±1.8 vs. 50.2±2.9 mL/kg−1. min−1, p<.001) compared the LH group. There was no main effect of group (OB-IR vs. LHC) on change in sRAGE or sRAGEc in response to exercise (ΔsRAGE 20.3±53.2 vs. 13.8±34.4 pg/mL, p=.93), (ΔsRAGEc 28.7±47.1 vs. 14.4±34.8 pg/mL, p=.33). However there was an effect of gender on the response to acute exercise. Males in both groups saw a significantly greater increase in plasma sRAGE (131.49±46.46 vs. −46.94±39.23 pg/mL, p<.05) and plasma sRAGEc (127.73±47.04 vs. −36.08±34.13 pg/mL, p<.05) compared to females. This study is the first to show that young healthy women and obese/insulin resistant women have an impaired ability to increase sRAGE plasma levels with acute aerobic exercise. Recent data has suggested that estrogen can exacerbate RAGE signaling as well as inhibit sRAGE production although the precise mechanism for this interaction is unclear and warrants further investigation.

d-allulose provides cardioprotective effect by attenuating cardiac mitochondrial dysfunction in obesity-induced insulin-resistant rats

2020 ◽  
Author(s):  
Wanpitak Pongkan ◽  
Kewarin Jinawong ◽  
Wasana Pratchayasakul ◽  
Thidarat Jaiwongkam ◽  
Sasiwan Kerdphoo ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Cardioprotective Effect ◽  
Insulin Resistant

Ticagrelor reverses the mitochondrial dysfunction through preventing accumulated autophagosomes-dependent apoptosis and ER stress in insulin-resistant H9c2 myocytes

2020 ◽  
Vol 469 (1-2) ◽  
pp. 97-107
Author(s):  
Yusuf Olgar ◽  
Erkan Tuncay ◽  
Deniz Billur ◽  
Aysegul Durak ◽  
Semir Ozdemir ◽  
...  
Keyword(s):  
Er Stress ◽  
Mitochondrial Dysfunction ◽  
Insulin Resistant

scholarly journals Metabolomic Response of Skeletal Muscle to Aerobic Exercise Training in Insulin Resistant Type 1 Diabetic Rats

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Michelle S. Dotzert ◽  
Michael R. Murray ◽  
Matthew W. McDonald ◽  
T. Dylan Olver ◽  
Thomas J. Velenosi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Diabetic Rats ◽  
Aerobic Exercise Training ◽  
Insulin Resistant
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