scholarly journals Association of Expression Levels of Clock Genes and Autophagy-Related Genes under Abnormal Light/Dark Cycle Stimulation in NAFLD Mice

2020 ◽  
Author(s):  
Zhu Zhu ◽  
Zhengyang Wang ◽  
Bo Qin ◽  
Songfeng Zhao ◽  
Huafei Wang ◽  
...  
Keyword(s):  
Circadian Rhythm ◽  
Sleep Disorder ◽  
High Fat Diet ◽  
Clock Genes ◽  
Lipid Deposition ◽  
High Fat ◽  
Dark Cycle ◽  
Alcoholic Fatty Liver ◽  
Expression Levels ◽  
Circadian Rhythm Sleep Disorder

Abstract Background: Environmental disorders of the circadian rhythms can lead to metabolism-related diseases or exacerbate pathological conditions. Non-alcoholic fatty liver disease (NAFLD) has emerged with a growing occurrence. In the present study, we attempted to indicate whether circadian clock may influence lipid deposition and the expression levels of autophagy-related genes in liver of mice. Methods: High-fat diet and abnormal light/dark cycles were employed to induce a mouse model of NAFLD with circadian rhythm sleep disorder. Herein, liver samples were obtained at ZT0, ZT4, ZT8, ZT12, ZT16, and ZT20 time-point to detect the rhythmic expressions of circadian genes, autophagy-related genes, and Rev-erbα. Results: Abnormal exposure to light aggravated lipid deposition in liver of mice and exacerbated disorders related to 24-h expression levels of clock genes, autophagy-related genes, and Rev-erbα. Besides, Rev-erbα could transcriptionally control the expression levels of autophagy-related genes. Conclusions: The long-term high-fat diet combined with abnormal light/dark cycle stimulation aggravated the development of NAFLD and disturbed the expressions levels of autophagy-related genes. An abnormal circadian expression may lead to NAFLD aggression. Besides, the abnormal expression levels of clock genes may create an association between circadian rhythm sleep disorder and autophagy.

Daily expression of clock genes in whole blood cells in healthy subjects and a patient with circadian rhythm sleep disorder

2005 ◽  
Vol 289 (5) ◽  
pp. R1273-R1279 ◽  
Author(s):  
Mieko Takimoto ◽  
Akinobu Hamada ◽  
Akemi Tomoda ◽  
Shigehiro Ohdo ◽  
Takafumi Ohmura ◽  
...  
Keyword(s):  
Circadian Rhythm ◽  
Sleep Disorder ◽  
Clinical Features ◽  
Whole Blood ◽  
Blood Cells ◽  
Clock Genes ◽  
Circadian Rhythm Sleep Disorders ◽  
Circadian Rhythm Sleep Disorder ◽  
Whole Blood Cells ◽  
Peak Phase

In recent years, circadian rhythm sleep disorders in humans have been increasing. Clinical features characteristic of this disorder are well known, but the specific causes remain unknown. However, various derangements of circadian expression of the clock gene are a probable cause of this disease. We have attempted to elucidate the relationship between the expression of the clock genes in whole blood cells and the clinical features characteristic of this disorder. In this study, we indicate the daily expression of clock genes period ( Per) 1, 2, 3, Bmal1, and Clock in whole blood cells in 12 healthy male subjects. The peak phase of Per1, Per2, and Per3 appeared in the early morning, whereas that of Bmal1 and Clock appeared in the midnight hours. Furthermore, in one patient case with circadian rhythm sleep disorder, we observed variations of the peak phase in clock genes by treatments such as light therapy, exercise therapy, and medicinal therapy. This study suggested that the monitoring of human clock genes in whole blood cells, which may be functionally important for the molecular control of the circadian pacemaker as well as in suprachiasmatic nucleus, might be useful to evaluate internal synchronization.

scholarly journals Su1545 – Differential Dna Methylation Status in Core Clock Genes Leads to Altered Circadian Rhythm in High-Fat Diet Fed Mice

2019 ◽  
Vol 156 (6) ◽  
pp. S-1293-S-1294
Author(s):  
Yuyan Han ◽  
Faith Cheplick ◽  
Nan Wu ◽  
Tianhao Zhou ◽  
Lindsey Kennedy ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Circadian Rhythm ◽  
High Fat Diet ◽  
Clock Genes ◽  
Methylation Status ◽  
High Fat

scholarly journals Admistration of Exogenous Melatonin Improves the Diurnal Rhythms of Gut Microbiota in High Fat Diet-Fed Mice

2019 ◽  
Author(s):  
Jie Yin ◽  
Yuying Li ◽  
Hui Han ◽  
Gang Liu ◽  
Xin Wu ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Circadian Clock ◽  
High Fat Diet ◽  
Serum Lipid ◽  
Clock Genes ◽  
Diurnal Rhythms ◽  
High Fat ◽  
Dark Cycle ◽  
Exogenous Melatonin ◽  
Circadian Clock Genes

AbstractMelatonin, a circadian hormone, has been reported to improve host lipid metabolism by reprogramming gut microbiota, which also exhibits rhythmicity in a light/dark cycle. However, the effect of admistartion of exogenous melatonin on the diurnal variation in gut microbiota in high fat diet (HFD)-fed mice is obscure. Here, we further confirmed the anti-obesogenic effect of melatonin on in mice feed with HFD for two weeks. Samples were collected every 4 h within a 24-h period and diurnal rhythms of clock genes expression (Clock, Cry1, Cry2, Per1, and Per2) and serum lipid indexes varied with diurnal time. Notably, Clock and triglycerides (TG) showed a marked rhythm only in the control and melatonin treated mice, but not in the HFD-fed mice. Rhythmicity of these parameters were similar between control and melatonin treated HFD mice compared with the HFD group, indicating an improvement of melatonin in the diurnal clock of host metabolism in HFD-fed mice. 16S rDNA sequencing showed that most microbiota exhibited a daily rhythmicity and the trends differentiated at different groups and different time points. We also identified several specific microbiota correlating with the circadian clock genes and serum lipid indexes, which might contribute the potential mechanism of melatonin in HFD-fed mice. Interestingly, administration of exogenous melatonin only at daytime exhibited higher resistance to HFD-induced lipid dysmetabolism than nighttime treatment companying with altered gut microbiota (Lactobacillus, Intestinimonas, and Oscillibacter). Importantly, the responses of microbiota transplanted mice to HFD feeding also varied at different transplanting times (8:00 and 16:00) and different microbiota donors. In summary, daily oscillations in the expression of circadian clock genes, serum lipid indexes, and gut microbiota, appears to be driven by a short-time feeding of an HFD. Administration of exogenous melatonin improved the compositions and diurnal rhythmicity of gut microbiota, which might be linked to host diurnal rhythm and metabolism.ImportancePrevious studies show that a circadian hormone, melatonin, involves in host lipid metabolism by reprogramming gut microbiota, which also exhibits rhythmicity in a light/dark cycle. However, the effect of melatonin drinking on the diurnal variation in gut microbiota in high fat diet-fed mice is obscure. Here, we found that 24-h oscillations were widely occurred in circadian clock genes, serum lipid indexes, and gut microbiota. Melatonin drinking improved the compositions and circadian rhythmicity of gut microbiota, which might be linked to host circadian rhythm and metabolism.

scholarly journals Maternal tadalafil therapy for fetal growth restriction prevents non-alcoholic fatty liver disease and adipocyte hypertrophy in the offspring

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Takuya Kawamura ◽  
Hiroaki Tanaka ◽  
Ryota Tachibana ◽  
Kento Yoshikawa ◽  
Shintaro Maki ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fetal Growth ◽  
Fetal Programming ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Control Group ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

AbstractWe aimed to investigate the effects of maternal tadalafil therapy on fetal programming of metabolic function in a mouse model of fetal growth restriction (FGR). Pregnant C57BL6 mice were divided into the control, L-NG-nitroarginine methyl ester (L-NAME), and tadalafil + L-NAME groups. Six weeks after birth, the male pups in each group were given a high-fat diet. A glucose tolerance test (GTT) was performed at 15 weeks and the pups were euthanized at 20 weeks. We then assessed the histological changes in the liver and adipose tissue, and the adipocytokine production. We found that the non-alcoholic fatty liver disease activity score was higher in the L-NAME group than in the control group (p < 0.05). Although the M1 macrophage numbers were significantly higher in the L-NAME/high-fat diet group (p < 0.001), maternal tadalafil administration prevented this change. Moreover, the epididymal adipocyte size was significantly larger in the L-NAME group than in the control group. This was also improved by maternal tadalafil administration (p < 0.05). Further, we found that resistin levels were significantly lower in the L-NAME group compared to the control group (p < 0.05). The combination of exposure to maternal L-NAME and a high-fat diet induced glucose impairment and non-alcoholic fatty liver disease. However, maternal tadalafil administration prevented these complications. Thus, deleterious fetal programming caused by FGR might be modified by in utero intervention with tadalafil.

The effects of quercetin on the expression of SREBP-1c mRNA in high-fat diet-induced NAFLD in mice

2021 ◽  
Vol 32 (4) ◽  
pp. 637-644
Author(s):  
Jamal Nasser Saleh Al-maamari ◽  
Mahardian Rahmadi ◽  
Sisca Melani Panggono ◽  
Devita Ardina Prameswari ◽  
Eka Dewi Pratiwi ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Inhibitory Effect ◽  
Pcr Analysis ◽  
Regulator Gene ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Reverse Transcription Pcr ◽  
Hematoxylin Eosin ◽  
Alcoholic Fatty Liver Disease

Abstract Objectives The study aimed to determine the effect of quercetin on the expression of primary regulator gene involved in lipogenesis and triglycerides synthesis in the liver, and the sterol regulatory binding protein-1c (SREBP-1c) mRNA in non-alcoholic fatty liver disease (NAFLD) with a high-fat diet (HFD) model. Methods Fifty-six Balb/c mice were divided into seven groups: standard feed; HFD; HFD and quercetin 50 mg/kg for 28 days; HFD and quercetin 100 mg/kg BW for 28 days; HFD and quercetin 50 mg/kg for 14 days; HFD and quercetin 100 mg/kg for 14 days; HFD and repaired fed for 14 days. Quercetin was administered intraperitoneally. The animals were sacrificed 24 h after the last treatment; the liver was taken for macroscopic, histopathological staining using hematoxylin–eosin and reverse transcription-PCR analysis sample. Results HFD significantly increased the expression of SREBP-1c mRNA; meanwhile, quercetin and repaired feed significantly reduced the expression of SREBP-1c mRNA in the liver. Quercetin at a dose of 50 mg/kg and 100 mg/kg also improved liver cells’ pathological profile in high-fat diet NAFLD. Conclusions The present study suggests that quercetin has an inhibitory effect on SREBP-1c expression and improved liver pathology in NAFLD mice.

scholarly journals Ezetimibe prevents the development of non-alcoholic fatty liver disease induced by high-fat diet in C57BL/6J mice

2014 ◽  
Vol 10 (6) ◽  
pp. 2917-2923 ◽  
Author(s):  
XIANG WANG ◽  
QIAOHUA REN ◽  
TAO WU ◽  
YONG GUO ◽  
YONG LIANG ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Triterpenoid-Rich Fraction from Ilex hainanensis Merr. Attenuates Non-Alcoholic Fatty Liver Disease Induced by High Fat Diet in Rats

2013 ◽  
Vol 41 (03) ◽  
pp. 487-502 ◽  
Author(s):  
Wei-Xi Cui ◽  
Jie Yang ◽  
Xiao-Qing Chen ◽  
Qian Mao ◽  
Xiang-Lan Wei ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Liver Disease ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Density Lipoprotein ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Cyp2e1 Expression ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) has become a major challenge to the healthcare system. This study was designed to evaluate the effect of the triterpenoid-rich fraction (TF) from Ilex hainanensis Merr. on NAFLD. Male Sprague-Dawley (SD) rats were fed a normal diet (control) or high fat diet (NAFLD model). After four weeks, the high fat diet group was orally administrated TF (250 mg/kg) for another two weeks. High fat diet fed rats displayed hyperlipidemia and a decline in liver function compared with control. However, administration with TF could effectively improve these symptoms, as demonstrated by decreasing the plasma levels of triglyceride (p <0.05), total cholesterol (p < 0.01), low-density lipoprotein cholesterol (p < 0.05), alanine transaminase (p < 0.05), aspartate aminotransferase (p < 0.01), liver index (p < 0.05) and insulin resistance index (p < 0.05) while increasing the high-density lipoprotein cholesterol (p < 0.05). Meanwhile, histopathological examination of livers also showed that TF could reduce the incidence of liver lesions induced by high fat diet. Furthermore, TF could alleviate oxidative stress and inflammation status indicated by the decline malondialdehyde and superoxide dismutase levels (p < 0.01, both) and levels of interleukin 6 and tumor necrosis factor-α (p < 0.05). In addition, immunohistochemistry showed TF evidently elevated the peroxisome proliferator-activated receptor (PPARα) expression (p < 0.01), while it diminished the Cytochrome P450 2E1 (CYP2E1) expression (p < 0.01) in liver. These results demonstrate that TF has potential ability to protect liver against NAFLD by regulating lipids metabolism and alleviating insulin resistance, inflammation and oxidative stress. This effect might be associated with regulating PPARα and CYP2E1 expression.

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