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

scholarly journals Vildagliptin and caloric restriction for cardioprotection in pre-diabetic rats

2017 ◽  
Vol 232 (2) ◽  
pp. 189-204 ◽  
Author(s):  
Pongpan Tanajak ◽  
Hiranya Pintana ◽  
Natthaphat Siri-Angkul ◽  
Juthamas Khamseekaew ◽  
Nattayaporn Apaijai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Cardiac Dysfunction ◽  
Metabolic Regulation ◽  
Left Ventricular ◽  
Lv Function ◽  
Insulin Resistant

Long-term high-fat diet (HFD) consumption causes cardiac dysfunction. Although calorie restriction (CR) has been shown to be useful in obesity, we hypothesized that combined CR with dipeptidyl peptidase-4 (DPP-4) inhibitor provides greater efficacy than monotherapy in attenuating cardiac dysfunction and metabolic impairment in HFD-induced obese-insulin resistant rats. Thirty male Wistar rats were divided into 2 groups to be fed on either a normal diet (ND, n = 6) or a HFD (n = 24) for 12 weeks. Then, HFD rats were divided into 4 subgroups (n = 6/subgroup) to receive just the vehicle, CR diet (60% of mean energy intake and changed to ND), vildagliptin (3 mg/kg/day) or combined CR and vildagliptin for 4 weeks. Metabolic parameters, heart rate variability (HRV), cardiac mitochondrial function, left ventricular (LV) and fibroblast growth factor (FGF) 21 signaling pathway were determined. Rats on a HFD developed insulin and FGF21 resistance, oxidative stress, cardiac mitochondrial dysfunction and impaired LV function. Rats on CR alone showed both decreased body weight and visceral fat accumulation, whereas vildagliptin did not alter these parameters. Rats in CR, vildagliptin and CR plus vildagliptin subgroups had improved insulin sensitivity and oxidative stress. However, vildagliptin improved heart rate variability (HRV), cardiac mitochondrial function and LV function better than the CR. Chronic HFD consumption leads to obese-insulin resistance and FGF21 resistance. Although CR is effective in improving metabolic regulation, vildagliptin provides greater efficacy in preventing cardiac dysfunction by improving anti-apoptosis and FGF21 signaling pathways and attenuating cardiac mitochondrial dysfunction in obese-insulin-resistant rats.

scholarly journals Aging induced by D-galactose aggravates cardiac dysfunction via exacerbating mitochondrial dysfunction in obese insulin-resistant rats

GeroScience ◽  
2019 ◽  
Vol 42 (1) ◽  
pp. 233-249 ◽  
Author(s):  
Cherry Bo-Htay ◽  
Thazin Shwe ◽  
Louis Higgins ◽  
Siripong Palee ◽  
Krekwit Shinlapawittayatorn ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Cardiac Dysfunction ◽  
Insulin Resistant

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

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

scholarly journals Effect of Chronic Treatment with Bovine Recombinant Growth Hormone on Cardiac Dysfunction and Lesion Progression in UM-X7.1 Cardiomyopathic Hamsters

Endocrinology ◽  
2002 ◽  
Vol 143 (12) ◽  
pp. 4846-4855 ◽  
Author(s):  
Sylvie Marleau ◽  
Nathalie Lapointe ◽  
Julie Massicotte ◽  
Catia Céméus ◽  
Gaëtan Jasmin ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Cardiac Dysfunction ◽  
Chronic Treatment ◽  
Recombinant Growth Hormone ◽  
Cardiomyopathic Hamsters

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.

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

scholarly journals Involvement of Mitochondrial Disorders in Septic Cardiomyopathy

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Arthur Durand ◽  
Thibault Duburcq ◽  
Thibault Dekeyser ◽  
Remi Neviere ◽  
Michael Howsam ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Cardiac Dysfunction ◽  
Host Response ◽  
Therapeutic Strategies ◽  
Future Research ◽  
Septic Cardiomyopathy ◽  
Research Directions ◽  
Life Threatening ◽  
Future Research Directions

Sepsis is defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection. It remains a leading cause of death worldwide, despite the development of various therapeutic strategies. Cardiac dysfunction, also referred to as septic cardiomyopathy, is a frequent and well-described complication of sepsis and associated with worse clinical outcomes. Recent research has increased our understanding of the role of mitochondrial dysfunction in the pathophysiology of septic cardiomyopathy. The purpose of this review is to present this evidence as a coherent whole and to highlight future research directions.

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