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

Tunapong, Wannipa; Apaijai, Nattayaporn; Yasom, Sakawdaurn; Tanajak, Pongpan; Wanchai, Keerati; Chunchai, Titikorn; Kerdphoo, Sasiwan; Eaimworawuthikul, Sathima; Thiennimitr, Parameth; Pongchaidecha, Anchalee; Lungkaphin, Anusorn; Pratchayasakul, Wasana; Chattipakorn, Nipon; Chattipakorn, Nipon

doi:10.1007/s00394-017-1482-3

Cited by 79 publications

(43 citation statements)

References 59 publications

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“…These data are in line with data produced previously (Zaitone and Essawy, 2012; Tunapong et al, 2018). In agreement, human studies highlighted a causal relationship between excessive caloric intake, weight gain, and tissue resistance to insulin (Delgado et al, 2018).…”

Section: Discussionsupporting

confidence: 92%

Pharmacological Action of a Pregnane Glycoside, Russelioside B, in Dietary Obese Rats: Impact on Weight Gain and Energy Expenditure

et al. 2018

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Background and purpose: Russelioside B (RB) is a pregnane glycoside obtained from Caralluma quadrangula; a herb with antidiabetic, anti-inflammatory, and antihyperlipidemic activities. The present experiment tested the possible role of RB in controlling weight gain in rats fed on high fat (HF) diet.Methods: RB was separated from the n-butanol fraction of the crude methanolic extract by chromatographic separation on a Si gel column according to the procedures described previously. The experiment of the biological assessment of RB used 32 male Wistar rats (4 groups, n = 8). Group 1 rats were fed with a palatable normal diet. Group 2, 3, and 4 were fed on HF diet for 16 weeks. Group 2 served as the HF diet control group while Group 3 and 4 received daily oral doses of RB (25 and 50 mg/kg) during the last four weeks. Animals’ parameters like weight gain, fasting level of blood sugar, serum lipids, and serum liver enzyme activities were measured. Liver or adipose tissue weight was divided by the rat’s body weight and multiplied by 100 to obtain the liver or adipose tissue index, respectively. Adipose tissues were processed for histopathological examination, measurement of mRNA expression of visfatin, leptin, adiponectin, uncoupling protein-1 (UCP-1), and carnitine palmitoyl transferase-1 (CPT-1). Furthermore, serum levels of insulin, interleukin-6 (IL-6), IL-1β, tumor necrosis factor-α (TNF-α), leptin, resistin, and adiponectin were assessed using ELISA kits.Results: Rats fed with the HF diet exhibited significant body weight gain, abnormal liver function, disturbed lipid profile, and greater serum level of pro-inflammatory cytokines in addition to greater insulin resistance, adipose tissue and liver indices. Further, rats fed with the HF diet displayed upregulations in the expression of visfatin and leptin with downregulations in the expression of adiponectin, UCP-1, and CPT-1 compared to normal rats. Interestingly, RB (25 or 50 mg/kg) favorably modulated the measured parameters.Conclusion: Data from this study documented the beneficial role of RB in diminishing weight gain, improving the inflammatory perturbations and energy expenditure in HF diet fed rats. Therefore, RB might be a promising candidate for obesity.

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Section: Discussionsupporting

confidence: 92%

Pharmacological Action of a Pregnane Glycoside, Russelioside B, in Dietary Obese Rats: Impact on Weight Gain and Energy Expenditure

et al. 2018

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“…Our previous studies have shown that 12 weeks of HFD consumption caused obese‐insulin resistance in rats . In addition, the HFD consumption is associated with cardiac autonomic imbalance, an increased blood pressure, leading to LV dysfunction . Similar to the HFD, there are studies reported that HFHS also caused obese‐insulin resistance and LV dysfunction, but it did not affect blood pressure in rodents …”

Section: Introductionmentioning

confidence: 98%

High‐Saturated Fat High‐Sugar Diet Accelerates Left‐Ventricular Dysfunction Faster than High‐Saturated Fat Diet Alone via Increasing Oxidative Stress and Apoptosis in Obese‐Insulin Resistant Rats

Apaijai

Arinno

Palee

et al. 2018

Molecular Nutrition Food Res

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Scope It has been hypothesized that a high‐saturated‐fat, high‐sugar diet (HFHS) causes worse cardiometabolic dysfunction than a high‐saturated‐fat diet (HFD) due to severe mitochondrial dysfunction, oxidative stress, and apoptosis in obese insulin‐resistant rats. Methods and Results Rats are divided into three groups to receive normal diet (ND), HFD, or HFHS for 24 weeks. Cardiometabolic parameters are determined at baseline and every 4 weeks until the end of the feeding protocol. At week 24, hearts are removed to determine mitochondrial function and dynamics, apoptosis, and insulin signaling. HFD and HFHS rats develop obese insulin‐resistance at week 8. However, fasting plasma glucose level is increased only in HFHS rats. Myocardial insulin signaling is markedly impaired in HFHS rats compared to other groups. Cardiac autonomic imbalance is observed in both HFD and HFHS rats beginning at week 8. However, cardiac dysfunction is observed earlier (week 8) in HFHS rats, and later at week 12 in HFD rats. Moreover, cardiac and mitochondrial oxidative stress levels, and apoptosis are greater in HFHS rats than HFD rats. Conclusion Both HFD and HFHS cause cardiometabolic dysfunction. HFHS causes more severe metabolic disturbance, oxidative stress, and apoptosis than HFD, which leads to an accelerated LV dysfunction in HFHS rats.

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“…Both red and green fluorescence intensity were measured by a fluorescence microplate reader (BioTek). Therefore, a decreased red/green fluorescent intensity ratio indicates mitochondrial membrane depolarization [18]. …”

Section: Methodsmentioning

confidence: 99%

“…They were then exposed to an enhanced chemiluminescent substrate (Clarity Western ECL Substrate; Bio-Rad). The Western blot images and densitometric analysis were carried out using the ChemiDoc Imaging system with Image Lab software (Bio-Rad) [16, 18]. …”

Section: Methodsmentioning

confidence: 99%

“…Then, the pressure-volume catheter was connected to the pressure-volume admittance system (ADV500; Transonic), and the signals were recorded via a Labscribe 2 program (iWorx, NH, USA). LV function including heart rate (HR), end-systolic and diastolic pressure (ESP, EDP), ±dP/dt, end-systolic and diastolic volume (ESV, EDV), and stroke volume (SV) were determined [18]. …”

Section: Methodsmentioning

confidence: 99%

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Testosterone Deprivation Aggravates Left-Ventricular Dysfunction in Male Obese Insulin-Resistant Rats via Impairing Cardiac Mitochondrial Function and Dynamics Proteins

et al. 2018

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Background: We have previously reported that testosterone deprivation at a very young age accelerated, but did not aggravate, left-ventricular (LV) dysfunction in obese insulin-resistant rats. However, the effects of testosterone deprivation during adulthood on LV function in obese insulin-resistant rats remains unclear. We hypothesized that testosterone deprivation aggravates LV dysfunction and cardiac autonomic imbalance via the impairment of cardiac mitochondrial function and dynamics proteins, a reduction in insulin receptor function, and an increase in apoptosis in obese insulin-resistant rats. Methods: Male rats were fed on either a normal diet (ND) or a high-fat diet (HFD) for 12 weeks. They were then subdivided into 2 groups: sham operation (NDS, HFS) and orchiectomy (NDO, HFO). Metabolic parameters, blood pressure, heart rate variability (HRV), and LV function were determined at baseline and before and after orchiectomy. Mitochondrial function and dynamics proteins, insulin signaling, and apoptosis were determined 12 weeks postoperatively. Results: HFS rats exhibited obese insulin resistance, depressed HRV, and LV dysfunction. In HFO rats, systolic blood pressure was increased with more excessive depression of HRV and increased LV dysfunction, compared with HFS rats. These adverse cardiac effects were consistent with markedly increased mitochondrial dysfunction, reduced mitochondrial complex I and III proteins, reduced mitochondrial fusion proteins, and increased apoptosis, compared with HFS rats. However, testosterone deprivation did not lead to any alteration in the insulin-resistant condition in HFO rats, compared with HFS rats. Conclusion: We concluded that testosterone deprivation during adulthood aggravated the impairment of mitochondrial function, mitochondrial respiratory complex, mitochondrial dynamics proteins, and apoptosis, leading to LV dysfunction in obese insulin-resistant rats.

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

Abstract: Prebiotics, probiotics, and synbiotics shared similar efficacy in reducing insulin resistance and LV dysfunction in obese insulin-resistant rats.

Cited by 79 publications

References 59 publications

Pharmacological Action of a Pregnane Glycoside, Russelioside B, in Dietary Obese Rats: Impact on Weight Gain and Energy Expenditure

Pharmacological Action of a Pregnane Glycoside, Russelioside B, in Dietary Obese Rats: Impact on Weight Gain and Energy Expenditure

High‐Saturated Fat High‐Sugar Diet Accelerates Left‐Ventricular Dysfunction Faster than High‐Saturated Fat Diet Alone via Increasing Oxidative Stress and Apoptosis in Obese‐Insulin Resistant Rats

Testosterone Deprivation Aggravates Left-Ventricular Dysfunction in Male Obese Insulin-Resistant Rats via Impairing Cardiac Mitochondrial Function and Dynamics Proteins

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