Gender-differences in the associations between circulating creatine kinase, blood pressure, body mass and non-alcoholic fatty liver disease in asymptomatic asians

Yen, Chih‐Hsuan; Wang, Kuang-Te; Lee, Ping-Ying; Liu, Chuan-Chuan; Hsieh, Ya‐Ching; Kuo, Jen‐Yuan; Bulwer, Bernard E.; Hung, Chung‐Lieh; Chang, Shun-Chuan; Shih, Shou‐Chuan; Hu, Kuang-Chun; Yeh, Hung‐I; Lam, Carolyn S.P.

doi:10.1371/journal.pone.0179898

Cited by 18 publications

(25 citation statements)

References 38 publications

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“…Cyp2b-null males also have slightly greater inflammatory responses based on RNA-seq data with no changes in CRP or corticosterone levels. CDAHFD-fed Cyp2b-null males also showed a 1.5-fold increase of serum creatine kinase levels compared to all other treatment groups, suggesting that CDAHFD treatment causes damage to Cyp2b-null males in other tissues, such as cardiac or skeletal muscle, in addition to liver [50].…”

Section: Plos Onementioning

confidence: 91%

“…Male mice fed a CDAHFD showed increased levels of serum ALT, AST, and ALP regardless of genotype (Fig 3B). CDAHFD-fed Cyp2b-null males had higher levels of creatine kinase (CK) (1.5-fold) compared to all other treatment groups including their WT counterparts, suggesting that Cyp2b-null males are more susceptible to CDAHFD-induced damage in other tissues such as cardiac and skeletal muscle [50], the opposite of females (Fig 3B).…”

Section: Plos Onementioning

confidence: 99%

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Gender differences in diet-induced steatotic disease in Cyp2b-null mice

et al. 2020

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Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease; however, progression to nonalcoholic steatohepatitis (NASH) is associated with most adverse outcomes. CYP2B metabolizes multiple xeno-and endobiotics, and male Cyp2b-null mice are dietinduced obese (DIO) with increased NAFLD. However, the DIO study was not performed long enough to assess progression to NASH. Therefore, to assess the role of Cyp2b in fatty liver disease progression from NAFLD to NASH, we treated wildtype (WT) and Cyp2b-null mice with a normal diet (ND) or choline-deficient, L-amino acid-defined high fat diet (CDAHFD) for 8 weeks and determined metabolic and molecular changes. CDAHFD-fed WT female mice gained more weight and had greater liver and white adipose tissue mass than their Cyp2b-null counterparts; males experienced diet-induced weight loss regardless of genotype. Serum biomarkers of liver injury increased in both CDAHFD-fed female and male mice; however CDAHFD-fed Cyp2b-null females exhibited significantly lower serum ALT, AST, and ASP concentrations compared to WT mice, indicating Cyp2b-null females were protected from liver injury. In both genders, hierarchical clustering of RNA-seq data demonstrates several gene ontologies responded differently in CDAHFD-fed Cyp2b-null mice compared to WT mice (lipid metabolism > fibrosis > inflammation). Oil Red O staining and direct triglycerides measurements confirmed that CDAHFD-fed Cyp2b-null females were protected from NAFLD. CDAHFD-fed Cyp2b-null mice showed equivocal changes in fibrosis with transcriptomic and serum markers suggesting less inflammation due to glucocorticoid-mediated repression of immune responses. In contrast to females, CDAHFD-fed Cyp2b-null males had higher triglyceride levels. Results indicate that female Cyp2b-null mice are protected from NAFLD while male Cyp2b-null mice are more susceptible to NAFLD, with few significant changes in NASH development. This study confirms that increased NAFLD development does not necessarily lead to progressive NASH. Furthermore, it indicates a role for Cyp2b in fatty liver disease that differs based on gender.

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Section: Plos Onementioning

confidence: 91%

Section: Plos Onementioning

confidence: 99%

Gender differences in diet-induced steatotic disease in Cyp2b-null mice

et al. 2020

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“…The study flow is depicted in Figure 2 and the included studies are in Table 1 [6,7,11,12,13,14,15,16,17,18,19]. We retrieved 135 reports from electronic databases and included 7 reports from 6 studies [6,7,11,15,16,17,19]. We additionally retrieved 4 papers through hand search [12,13,14,18], 3 of which were not included in electronic databases [12,13,18].…”

Section: Resultsmentioning

confidence: 99%

“…We additionally retrieved 4 papers through hand search [12,13,14,18], 3 of which were not included in electronic databases [12,13,18]. In total, we included 11 papers from 10 studies [6,7,11,12,13,14,15,16,17,18,19].…”

Section: Resultsmentioning

confidence: 99%

Creatine Kinase and Blood Pressure: A Systematic Review

Brewster¹,

Karamat

Montfrans

2019

Medical Sciences

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Background: Hypertension is a main risk factor for premature death. Although blood pressure is a complex trait, we have shown that the activity of the ATP-generating enzyme creatine kinase (CK) is a significant predictor of blood pressure and of failure of antihypertensive drug therapy in the general population. In this report, we systematically review the evidence on the association between this new risk factor CK and blood pressure outcomes. Method: We used a narrative synthesis approach and conducted a systematic search to include studies on non-pregnant adult humans that address the association between plasma CK and blood pressure outcomes. We searched electronic databases and performed a hand search without language restriction. We extracted data in duplo. The main outcome was the association between CK and blood pressure as continuous measures. Other outcomes included the association between CK and blood pressure categories (normotension and hypertension, subdivided in treated controlled, treated uncontrolled, and untreated hypertension). Results: We retrieved 139 reports and included 11 papers from 10 studies assessing CK in 34,578 participants, men and women, of African, Asian, and European ancestry, aged 18 to 87 years. In 9 reports, CK was associated with blood pressure levels, hypertension (vs. normotension), and/or treatment failure. The adjusted increase in systolic blood pressure (mmHg/log CK increase) was reported between 3.3 [1.4 to 5.2] and 8.0 [3.3 to 12.7] and the odds ratio of hypertension with high vs. low CK ranged between 1.2 and 3.9. In addition, CK was a strong predictor of treatment failure in the general population, with an adjusted odds ratio of 3.7 [1.2 to 10.9]. Discussion: This systematic review largely confirms earlier reports that CK is associated with blood pressure and failure of antihypertensive therapy. Further work is needed to address whether this new risk factor is useful in clinical medicine.

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“…Non-alcoholic fatty liver disease (NAFLD) is a disorder of excessive fat accumulation (steatosis) in the liver of those who consume little to no alcohol [1,2]. With the increase of rich foods in the diets of Western counties and developing countries around the world, NAFLD has become a rising cause of hepatic steatosis since its first reported in 1983 [3][4][5]. Up to 25% of adults in the United States has NAFLD, with more than 80% of the obese population affected by the disease.…”

Section: Introductionmentioning

confidence: 99%

Nonalcoholic fatty liver disease experiences accumulation of hepatic liquid crystal associated with increasing lipophagy

Wang

Jones

et al. 2020

Cell Biosci

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Background: In the past 30 years, incidences of non-alcoholic fatty liver disease (NAFLD) has risen by 30%. However, there is still no clear mechanism or accurate method of anticipating liver failure. Here we reveal the phase transitions of liquid crystalline qualities in hepatic lipid droplets (HLDs) as a novel method of anticipating prognosis. Methods: NAFLD was induced by feeding C57BL/6J mice on a high-fat (HiF) diet. These NAFLD livers were then evaluated under polarized microscopy, X-ray diffraction and small-angle scattering, lipid component chromatography analysis and protein expression analysis. Optically active HLDs from mouse model and patient samples were both then confirmed to have liquid crystal characteristics. Liver MAP1LC3A expression was then evaluated to determine the role of autophagy in liquid crystal HLD (LC-HLD) formation. Results: Unlike the normal diet cohort, HiF diet mice developed NAFLD livers containing HLDs exhibiting Maltese cross birefringence, phase transition, and fluidity signature to liquid crystals. These LC-HLDs transitioned to anisotropic crystal at 0 °C and remain crystalline. Temperature increase to 42 °C causes both liquid crystal and crystal HLDs to convert to isotropic droplet form. These isotropic HLDs successfully transition to anisotropic LC with fast temperature decrease and anisotropic crystal with slow temperature decrease. These findings were duplicated in patient liver. Patient LC-HLDs with no inner optical activity were discovered, hinting at lipid saturation as the mechanism through which HLD acquire LC characteristics. Downregulation of MAP1LC3A in conjunction with increased LC-HLD also implicated autophagy in NAFLD LC-HLD formation. Conclusions: Increasing concentrations of amphiphilic lipids in HLDs favors organization into alternating hydrophilic and hydrophobic layers, which present as LC-HLDs. Thus, evaluating the extent of liquid crystallization with phase transition in HLDs of NAFLD patients may reveal disease severity and predict impending liver damage.

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Gender-differences in the associations between circulating creatine kinase, blood pressure, body mass and non-alcoholic fatty liver disease in asymptomatic asians

Cited by 18 publications

References 38 publications

Gender differences in diet-induced steatotic disease in Cyp2b-null mice

Gender differences in diet-induced steatotic disease in Cyp2b-null mice

Creatine Kinase and Blood Pressure: A Systematic Review

Nonalcoholic fatty liver disease experiences accumulation of hepatic liquid crystal associated with increasing lipophagy

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