Effects of pioglitazone on cardiac and adipose tissue pathology in rats with metabolic syndrome

Matsuura, Natsumi; Asano, Chiharu; Nagasawa, Kai; Ito, Shogo; Sano, Yusuke; Minagawa, Yuji; Yamada, Yoshio; Hattori, Takuya; Watanabe, Shozo; Murohara, Toyoaki; Nagata, Kazuya

doi:10.1016/j.ijcard.2014.11.099

Cited by 38 publications

(37 citation statements)

References 55 publications

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“…We found in the hearts of our obese Zucker rats that AMPK protein expression was not affected; however, phosphorylation at Thr127, an indication of AMPK activity, was reduced. This is in agreement with studies in hearts of obese ob / ob mice (Wang & Unger, ), and the crossover model of obese Dahl salt‐sensitive/Zucker rats (Matsuura et al., ), and suggests a disturbed cardiac energy homeostasis. Moreover, others did find a reduced AMPK protein expression in diet‐induced obese mice (Ko et al., ) or rats (Lindholm et al., ), although in obese Ossabaw swine no changes in protein expression or phosphorylation of AMPK were observed (Moberly et al., ).…”

Section: Discussionsupporting

confidence: 91%

Cardiac β‐adrenergic responsiveness of obese Zucker rats: The role of AMPK

Bussey

Thaung

Hughes

et al. 2018

Experimental Physiology

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The obesity epidemic impacts heavily on cardiovascular health, in part owing to changes in cardiac metabolism. AMP-activated protein kinase (AMPK) is a key regulator of energy homeostasis in the heart and is regulated by β-adrenoceptors (β-ARs) in normal conditions. In obesity, chronic sympathetic overactivation leads to impaired cardiac β-AR responsiveness, although it is unclear whether AMPK signalling, downstream of β-ARs, contributes to this dysfunction. Therefore, we aimed to determine whether reduced AMPK signalling is responsible for the reduced β-AR responsiveness in obesity. In isolated hearts of lean and obese Zucker rats, we tested β-AR responsiveness to the β -AR agonist isoprenaline (ISO, 1 × 10 to 5 × 10 m) in the absence and presence of the AMPK inhibitor, compound C (CC, 10 μm). The β -AR expression and AMPK phosphorylation were assessed by Western blot. β-Adrenergic responsiveness was reduced in the hearts of obese rats (logEC of ISO-developed pressure dose-response curves: lean -8.53 ± 0.13 × 10 m versus obese -8.35 ± 0.10 × 10 m ; P < 0.05 lean versus obese, n = 6 per group). This difference was not apparent after AMPK inhibition (logEC of ISO-developed pressure curves: lean CC -8.19 ± 0.12 × 10 m versus obese CC 8.17 ± 0.13 × 10 m, P < 0.05, n = 6 per group). β -Adrenergic receptor expression and AMPK phosphorylation were reduced in hearts of obese rats (AMPK at Thr : lean 1.73 ± 0.17 a.u. versus lean CC 0.81 ± 0.13 a.u., and obese 1.18 ± 0.09 a.u. versus obese CC 0.81 ± 0.16 a.u., P < 0.05, n = 6 per group). Thus, a direct functional link between β-adrenergic responsiveness and AMPK signalling in the heart exists, and AMPK might be an important target to restore the reduced cardiac β-adrenergic responsiveness in obesity.

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Section: Discussionsupporting

confidence: 91%

Cardiac β‐adrenergic responsiveness of obese Zucker rats: The role of AMPK

Bussey

Thaung

Hughes

et al. 2018

Experimental Physiology

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“…In animal production, growth performance is one of the most important indexes for evaluating the efficiency of additives. Previous studies have found that a diet supplemented with PGZ could increase feed intake in pigs and rats . Moreover, some studies have also shown that PGZ supplementation increased body weight in male mice and the ADG in finishing pigs .…”

Section: Discussionmentioning

confidence: 97%

Dietary supplementation with pioglitazone hydrochloride improves intramuscular fat, fatty acid profile, and antioxidant ability of thigh muscle in yellow‐feathered chickens

et al. 2019

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BACKGROUND Muscle fat content and fatty acid composition play an important role in poultry flavor and taste. To investigate the effects of pioglitazone hydrochloride (PGZ) on growth performance and thigh muscle quality in yellow‐feathered chickens, 360 female chickens were randomly divided into three groups and treated with three doses of PGZ (0, 7.5, and 15 mg kg−1) for 28 days. Each group had six replicates of 20 chickens. RESULTS The results showed that dietary supplementation with 15 mg kg−1 PGZ increased average daily feed intake (ADFI) and the average daily gain (ADG) from 0 to 14 days. Furthermore, the triglyceride (TG) level was decreased by 15 mg kg−1 PGZ, whereas the eviscerated yield was increased. The relative weight of the heart and kidneys showed a linear increase with dietary PGZ supplementation, and the drip loss of the thigh muscle was significantly decreased by 15 mg kg−1 PGZ supplementation. Moreover, a* value, intramuscular fat (IMF), and polyunsaturated fatty acids (PUFAs) showed a linear increase, and pH24 h and drip loss showed a quadratic influence with the levels of PGZ supplementation. In particular, the PUFA proportion was increased by 7.63% and 9.14% in the 7.5 mg kg−1 PGZ and 15 mg kg−1 PGZ groups, respectively. Additionally, 15 mg kg−1 of PGZ increased the total antioxidant capacity (T‐AOC) and glutathione peroxidase (GSH‐PX) activity. CONCLUSION In summary, 15 mg kg−1 PGZ has substantial effects on growth performance and meat quality, particularly by decreasing drip loss and increasing IMF content, PUFA proportions, and antioxidant ability. © 2019 Society of Chemical Industry

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“…Portions of RNA (2 g) were subjected to reverse transcription with the use of a PrimerScript RT Reagent Kit (Takara, Shiga, Japan). Quantitative PCR analysis was performed with the use of SYBR Mix Ex Taq II (Takara), a Thermal Cycler Dice Real Time System II (Takara), and specific primers for cDNAs encoding atrial natriuretic peptide (29), brain natriuretic peptide (29), collagen types I or III (38), connective tissue growth factor (28), transforming growth factor-␤ 1 (29), monocyte chemoattractant protein (MCP)-1 (28), osteopontin (28), cyclooxygenase (COX)-2 (25), angiotensin-converting enzyme (29), ANG II type 1A receptor (8), mineralocorticoid receptor (MR) (29), serumand glucocorticoid-regulated kinase 1 (8), glucocorticoid receptor (GR) (22), 11␤-hydroxysteroid dehydrogenase type 1 (11␤-HSD1) (22), brain-derived neurotrophic factor (BDNF; forward: 5=-GCCCAACGAAGAAAACCATAAG-3= and reverse: 5=-AGTTTCTGGTTGCTGTGCTGTAAG-3=, GenBank Accession No. NM_001270630), and the p22 phox (51), gp91 phox (51), and Rac1 (24) subunits of NADPH oxidase.…”

Section: Methodsmentioning

confidence: 99%

Restraint stress exacerbates cardiac and adipose tissue pathology via β-adrenergic signaling in rats with metabolic syndrome

Matsuura

Nagasawa

Minagawa

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Restraint stress stimulates sympathetic nerve activity and can affect adiposity and metabolism. However, the effects of restraint stress on cardiovascular and metabolic disorders in metabolic syndrome (MetS) have remained unclear. We investigated the effects of chronic restraint stress and β-adrenergic receptor (β-AR) blockade on cardiac and adipose tissue pathology and metabolic disorders in a rat model of MetS. DahlS.Z-Lepr(fa)/Lepr(fa) (DS/obese) rats, derived from a cross between Dahl salt-sensitive and Zucker rats. Rats were exposed to restraint stress (restraint cage, 2 h/day) for 4 wk from 9 wk of age with or without daily subcutaneous administration of the β-AR blocker propranolol (2 mg/kg). Age-matched homozygous lean littermates of DS/obese rats (DahlS.Z-Lepr(+)/Lepr(+) rats) served as control animals. Chronic restraint stress exacerbated hypertension as well as left ventricular hypertrophy, fibrosis, diastolic dysfunction, and oxidative stress in a manner sensitive to propranolol treatment. Restraint stress attenuated body weight gain in DS/obese rats, and this effect tended to be reversed by propranolol (P = 0.0682). Restraint stress or propranolol did not affect visceral or subcutaneous fat mass. However, restraint stress potentiated cardiac and visceral adipose tissue inflammation in DS/obese rats, and these effects were ameliorated by propranolol. Restraint stress also exacerbated glucose intolerance, insulin resistance, and abnormal lipid metabolism in a manner sensitive to propranolol. In addition, restraint stress increased urinary norepinephrine excretion, and propranolol attenuated this effect. Our results thus implicate β-ARs in the exacerbation of cardiac and adipose tissue pathology and abnormal glucose and lipid metabolism induced by restraint stress in this model of MetS.

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Effects of pioglitazone on cardiac and adipose tissue pathology in rats with metabolic syndrome

Cited by 38 publications

References 55 publications

Cardiac β‐adrenergic responsiveness of obese Zucker rats: The role of AMPK

Cardiac β‐adrenergic responsiveness of obese Zucker rats: The role of AMPK

Dietary supplementation with pioglitazone hydrochloride improves intramuscular fat, fatty acid profile, and antioxidant ability of thigh muscle in yellow‐feathered chickens

Restraint stress exacerbates cardiac and adipose tissue pathology via β-adrenergic signaling in rats with metabolic syndrome

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