Global Transcriptomic Profiling of Cardiac Hypertrophy and Fatty Heart Induced by Long-Term High-Energy Diet in Bama Miniature Pigs

Xia, Ji‐Han; Zhang, Yuanyuan; Xin, Leilei; Kong, Siyuan; Chen, Yaoxing; Yang, Shulin; Li, Kui

doi:10.1371/journal.pone.0132420

Cited by 26 publications

(23 citation statements)

References 40 publications

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“…Xia et al fed a HFHSD to Bama minipigs to induce obesity [36]. They found that these obese pigs developed the metabolic syndrome, and showed cardiac steatosis and hypertrophy.…”

Section: Discussionmentioning

confidence: 99%

The high-fat diet induces myocardial fibrosis in the metabolically healthy obese minipigs—The role of ER stress and oxidative stress

Liu

Chu

et al. 2017

Clinical Nutrition

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“…Xia et al fed a HFHSD to Bama minipigs to induce obesity [36]. They found that these obese pigs developed the metabolic syndrome, and showed cardiac steatosis and hypertrophy.…”

Section: Discussionmentioning

confidence: 99%

The high-fat diet induces myocardial fibrosis in the metabolically healthy obese minipigs—The role of ER stress and oxidative stress

Liu

Chu

et al. 2017

Clinical Nutrition

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“…Early activation of STAT3 is evident in the heart in response to β-adrenergic receptor agonist treatment and cardiac specific STAT3 deletion led to increased cardiac hypertrophy, necrosis, and apoptosis after chronic β-adrenergic stimulation [13]. Obesity also has effects on cardiac STAT3 expression, in that cardiac STAT3 expression was differentially regulated in Bama miniature pigs fed a long-term high-energy diet compared to controls [14]. The suppressor of the cytokine signaling family (SOCS3) acts as a negative regulator of STAT3 [15].…”

Section: Introductionmentioning

confidence: 99%

High fat diet-induced obesity increases myocardial injury and alters cardiac STAT3 signaling in mice after polymicrobial sepsis

DeMartini

Nowell

James

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Little is known about how obesity affects the heart during sepsis and we sought to investigate the obesity-induced cardiac effects that occur during polymicrobial sepsis. Six-week old C57BL/6 mice were randomized to a high fat (HFD) (60% kcal fat) or normal diet (ND) (16% kcal fat). After 6 wks of feeding, mice were anesthetized with isoflurane and polymicrobial sepsis was induced by cecal ligation and puncture (CLP). Plasma and cardiac tissue were obtained for analysis. Echocardiography was performed on a separate cohort of mice at 0 and 18h after CLP. Following 6-wks of dietary intervention, plasma cardiac troponin I was elevated in obese mice at baseline compared to non-obese mice but troponin increased only in non-obese septic mice. IL-17a expression was 27-fold higher in obese septic mice versus non-obese septic mice. Cardiac phosphorylation of STAT3 at Ser727 was increased at baseline in obese mice and increased further only in obese septic mice. Phosphorylation of STAT3 at Tyr705 was similar in both groups at baseline and increased after sepsis. SOCS3, a downstream protein and negative regulator of STAT3, was elevated in obese mice at baseline compared to non-obese mice. After sepsis non-obese mice had an increase in SOCS3 expression that was not observed in obese mice. Taken together, we show that obesity affects cardiac function and leads to cardiac injury. Furthermore, myocardial injury in obese mice during sepsis may occur through alteration of the STAT3 pathway.

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“…4C. The kidneys and hearts of the 320 animals in the Tg HFHS group also weighed significantly more (p<0.01) than those of the 321 animals in the other groups, similar to findings reported in previous research using a miniature 322 pig model of early-stage diabetes Xia et al 2015). Table 1.…”

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Supplemental Information 2: Supplemental Raw Figures for Figure 1 PCR

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K. 2018. Kill two birds with one stone: making multi-transgenic pre-diabetes mouse models through insulin resistance and pancreatic apoptosis pathogenesis. PeerJ 6:e4542 https://doi.org/10.7717/peerj.4542Kill two birds with one stone: making multi-transgenic prediabetes mouse models through insulin resistance and pancreatic apoptosis pathogenesis Background. Type 2 diabetes, a chronic disease to which susceptibility is hereditary, is characterized by insulin resistance accompanied by defective insulin secretion. Mouse models, especially transgenic mice, play an important role in medical research. However, the transgenic mouse models that have been used in diabetes research are involved with single transgenes, focusing on the insulin gene or its mutants. Thus they mainly provide information related to Type 1 diabetes.Methods. Here, we attempted to focus comprehensively on genes related to pancreatic islet damage, peripheral insulin resistance and related environmental inducing factors by generating single-transgenic mice (CHOP), dual-transgenic mice (hIAPP-CHOP) and triple-transgenic mice (11β-HSD1-hIAPP-CHOP). The latter two types of transgenic animals were induced with high-fat, high-sucrose diets (HFHSD). We evaluated and analyzed the diabetes-related symptoms and the histopathological and immunohistochemical features of the transgenic animals.Results. Specifically, in the triple-transgene animals, the results of intraperitoneal glucose tolerance tests (IPGTT) began to change 60 days after induction (p<0.001). After 190 days of induction, the body weights (p<0.01) and plasma glucose levels of the animals in the Tg group were higher than those of the animals in the Nc group. After the mice were sacrificed, large amounts of lipid were found deposited in the adipose tissues (p<0.01) and ectopically deposited in the non-adipose tissues (p<0.05 or 0.01) of the animals in the Tg HFHSD group. The weights of the kidneys and hearts of the Tg animals were significantly increased (p<0.01). Serum C-P was decreased due to transgene effects, and insulin levels were increased due to the effects of the high-fat high-sucrose diet in the Tg HFHSD group, indicating that damaged insulin secretion and insulin resistance hyperinsulinemia existed simultaneously in these animals. The serum corticosterone levels of the animals in the Tg group were slightly higher than those of the Nc animals due to the effects of the 11βHSD-1 transgene and obesity. In the Tg HFHSD group, hepatic adipose deposition was more severe and the pancreatic islet area was enlarged under compensation, accompanying apoptosis. In the Tg ControlD group, hepatic adipose deposition was also severe, pancreatic islets were damaged, and their areas were decreased (p<0.05), and apoptosis of pancreatic cells occurred. Taken together, these data show that the transgenes led to early-stage pathological changes characteristic of type 2 diabetes in the triple-transgene HFHSD group. The disease of triple-transgenic mice was more severe than that of dual or single-transgenic ...

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Global Transcriptomic Profiling of Cardiac Hypertrophy and Fatty Heart Induced by Long-Term High-Energy Diet in Bama Miniature Pigs

Cited by 26 publications

References 40 publications

The high-fat diet induces myocardial fibrosis in the metabolically healthy obese minipigs—The role of ER stress and oxidative stress

The high-fat diet induces myocardial fibrosis in the metabolically healthy obese minipigs—The role of ER stress and oxidative stress

High fat diet-induced obesity increases myocardial injury and alters cardiac STAT3 signaling in mice after polymicrobial sepsis

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