Alleviation of hepatic fat accumulation by betaine involves reduction of homocysteine via up-regulation of betaine-homocysteine methyltransferase (BHMT)

2016 ◽  
Vol 477 (3) ◽  
pp. 440-447 ◽  
Author(s):  
Chul Won Ahn ◽  
Doo Sung Jun ◽  
Jong Deok Na ◽  
Yeo Jin Choi ◽  
Young Chul Kim
Keyword(s):  
Fat Accumulation ◽  
Hepatic Fat ◽  
Betaine Homocysteine Methyltransferase ◽  
Homocysteine Methyltransferase

Fenofibrate, a PPARα agonist, reduces hepatic fat accumulation through the upregulation of TFEB-mediated lipophagy

Metabolism ◽  
2021 ◽  
pp. 154798
Author(s):  
Jin Yoo ◽  
In-Kyung Jeong ◽  
Kyu Jeung Ahn ◽  
Ho Yeon Chung ◽  
You-Cheol Hwang
Keyword(s):  
Fat Accumulation ◽  
Hepatic Fat ◽  
Pparα Agonist

scholarly journals Vascular Adhesion Protein 1 Mediates Gut Microbial Flagellin-Induced Inflammation, Leukocyte Infiltration, and Hepatic Steatosis

Sci ◽  
2021 ◽  
Vol 3 (1) ◽  
pp. 13
Author(s):  
Raine Toivonen ◽  
Sanja Vanhatalo ◽  
Maija Hollmén ◽  
Eveliina Munukka ◽  
Anniina Keskitalo ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Hepatic Steatosis ◽  
Visceral Adipose Tissue ◽  
Leukocyte Infiltration ◽  
Fat Accumulation ◽  
Adhesion Protein ◽  
Hepatic Fat ◽  
Vascular Adhesion ◽  
Visceral Adipose ◽  
Vascular Adhesion Protein 1

Toll-like receptor 5 ligand, flagellin, and vascular adhesion protein 1 (VAP-1) are involved in non-alcoholic fatty liver disease. This study aimed to determine whether VAP-1 mediates flagellin-induced hepatic fat accumulation. The effects of flagellin on adipocyte VAP-1 expression were first studied in vitro. Then, flagellin (100 ng/mouse) or saline was intraperitoneally injected into C57BL/6J (WT) and C57BL/6-Aoc3-/- (VAP-1 KO) mice on a high-fat diet twice a week every 2 weeks for 10 weeks. After that, the effects on inflammation, insulin signaling, and metabolism were studied in liver and adipose tissues. Hepatic fat was quantified histologically and biochemically. Because flagellin challenge increased VAP-1 expression in human adipocytes, we used VAP-1 KO mice to determine whether VAP-1 regulates the inflammatory and metabolic effects of flagellin in vivo. In mice, VAP-1 mediated flagellin-induced inflammation, leukocyte infiltration, and lipolysis in visceral adipose tissue. Consequently, an increased release of glycerol led to hepatic steatosis in WT, but not in KO mice. Flagellin-induced hepatic fibrosis was not mediated by VAP-1. VAP-1 KO mice harbored more inflammation-related microbes than WT mice, while flagellin did not affect the gut microbiota. Our results suggest that by acting on visceral adipose tissue, flagellin increased leukocyte infiltration that induced lipolysis. Further, the released glycerol participated in hepatic fat accumulation. In conclusion, the results describe that gut microbial flagellin through VAP-1 induced hepatic steatosis.

scholarly journals Alanine Aminotransferase Levels and Fatty Liver in Childhood Obesity: Associations with Insulin Resistance, Adiponectin, and Visceral Fat

2006 ◽  
Vol 91 (11) ◽  
pp. 4287-4294 ◽  
Author(s):  
Tania S. Burgert ◽  
Sara E. Taksali ◽  
James Dziura ◽  
T. Robin Goodman ◽  
Catherine W. Yeckel ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Insulin Sensitivity ◽  
Fatty Liver ◽  
Visceral Fat ◽  
Resonance Imaging ◽  
Fat Accumulation ◽  
Glucose And Lipid Metabolism ◽  
The Metabolic Syndrome ◽  
Hepatic Fat ◽  
Fat Fraction

Abstract Background: Concurrent with the rise in obesity, nonalcoholic fatty liver disease is recognized as the leading cause of serum aminotransferase elevations in obese youth. Nevertheless, the complete metabolic phenotype associated with abnormalities in biomarkers of liver injury and intrahepatic fat accumulation remains to be established. Methods: In a multiethnic cohort of 392 obese adolescents, alanine aminotransferase (ALT) levels were related with parameters of insulin sensitivity, glucose, and lipid metabolism as well as adipocytokines and biomarkers of inflammation. A subset of 72 adolescents had determination of abdominal fat partitioning and intrahepatic fat accumulation using magnetic resonance imaging. Findings: Elevated ALT (>35 U/liter) was found in 14% of adolescents, with a predominance of male gender and white/Hispanic race/ethnicity. After adjusting for potential confounders, rising ALT was associated with reduced insulin sensitivity and glucose tolerance as well as rising free fatty acids and triglycerides. Worsening of glucose and lipid metabolism was already evident as ALT levels rose into the upper half of the normal range (18–35 U/liter). When hepatic fat fraction was assessed using fast magnetic resonance imaging, 32% of subjects had an increased hepatic fat fraction, which was associated with decreased insulin sensitivity and adiponectin, and increased triglycerides, visceral fat, and deep to superficial sc fat ratio. The prevalence of the metabolic syndrome was significantly greater in those with fatty liver. Interpretation: Deterioration in glucose and lipid metabolism is associated even with modest ALT elevations. Hepatic fat accumulation in childhood obesity is strongly associated with the triad of insulin resistance, increased visceral fat, and hypoadiponectinemia. Hence, hepatic steatosis may be a core feature of the metabolic syndrome.

Betaine: a key modulator of one-carbon metabolism and homocysteine status

2005 ◽  
Vol 43 (10) ◽  
Author(s):  
Per Magne Ueland ◽  
Pål I. Holm ◽  
Steinar Hustad
Keyword(s):  
Carbon Metabolism ◽  
Individual Variability ◽  
Vitamin B ◽  
Total Homocysteine ◽  
Altered Metabolism ◽  
One Carbon Metabolism ◽  
And Gender ◽  
Betaine Homocysteine Methyltransferase ◽  
Plasma Total Homocysteine ◽  
Homocysteine Methyltransferase

AbstractBetaine serves as a methyl donor in a reaction converting homocysteine to methionine, catalysed by the enzyme betaine-homocysteine methyltransferase. It has been used for years to lower the concentration of plasma total homocysteine (tHcy) in patients with homocystinuria, and has recently been shown to reduce fasting and in particular post-methionine load (PML) tHcy in healthy subjects.Betaine exists in plasma at concentrations of about 30μmol/L; it varies 10-fold (from 9 to 90μmol/L) between individuals, but the intra-individual variability is small. Major determinants are choline, dimethylglycine and folate in plasma, folic acid intake and gender.Recent studies have demonstrated that plasma betaine is a stronger determinant of PML tHcy than are vitamin BTo conclude, betaine status is a component of an individual's biochemical make-up with ramifications to one-carbon metabolism. Betaine status should be investigated in pathologies related to altered metabolism of homocysteine and folate, including cardiovascular disease, cancer and neural tube defects.

Jaboticaba peel powder and jaboticaba peel aqueous extract reduces obesity, insulin resistance and hepatic fat accumulation in rats

2019 ◽  
Vol 120 ◽  
pp. 880-887 ◽  
Author(s):  
Sabrina Alves Lenquiste ◽  
Celina de Almeida Lamas ◽  
Rafaela da Silva Marineli ◽  
Érica Aguiar Moraes ◽  
Patrícia Cristine Borck ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Aqueous Extract ◽  
Fat Accumulation ◽  
Hepatic Fat

Betaine homocysteine methyltransferase (BHMT) as a specific and sensitive blood marker for acute liver injury

Biomarkers ◽  
2014 ◽  
Vol 19 (7) ◽  
pp. 578-584 ◽  
Author(s):  
Huailei Ma ◽  
Jing Ning ◽  
Xin Jin ◽  
Chunming Mao ◽  
Xiangli Bu ◽  
...  
Keyword(s):  
Liver Injury ◽  
Acute Liver Injury ◽  
Blood Marker ◽  
Betaine Homocysteine Methyltransferase ◽  
Homocysteine Methyltransferase

scholarly journals Short-term strength training reduces gluconeogenesis and NAFLD in obese mice

2019 ◽  
Vol 241 (1) ◽  
pp. 59-70 ◽  
Author(s):  
Rodrigo Martins Pereira ◽  
Kellen Cristina da Cruz Rodrigues ◽  
Chadi Pellegrini Anaruma ◽  
Marcella Ramos Sant’Ana ◽  
Thaís Dantis Pereira de Campos ◽  
...  
Keyword(s):  
Weight Loss ◽  
Insulin Sensitivity ◽  
Strength Training ◽  
Term Strength ◽  
Obese Mice ◽  
Short Term ◽  
Fat Accumulation ◽  
Hepatic Insulin Sensitivity ◽  
Short Term Strength ◽  
Hepatic Fat

Non-alcoholic fatty liver disease (NAFLD) has a positive correlation with obesity, insulin resistance and type 2 diabetes mellitus (T2D). The aerobic training is an important tool in combating NAFLD. However, no studies have demonstrated the molecular effects of short-term strength training on the accumulation of hepatic fat in obese mice. This study aimed to investigate the effects of short-term strength training on the mechanisms of oxidation and lipid synthesis in the liver of obese mice. The short duration protocol was used to avoid changing the amount of adipose tissue. Swiss mice were separated into three groups: lean control (CTL), sedentary obese (OB) and strength training obese (STO). The obese groups were fed a high-fat diet (HFD) and the STO group performed the strength training protocol 1 session/day for 15 days. The short-term strength training reduced hepatic fat accumulation, increasing hepatic insulin sensitivity and controlling hepatic glucose production. The obese animals increased the mRNA of lipogenic genes Fasn and Scd1 and reduced the oxidative genes Cpt1a and Ppara. On the other hand, the STO group presented the opposite results. Finally, the obese animals presented higher levels of lipogenic proteins (ACC and FAS) and proinflammatory cytokines (TNF-α and IL-1β), but the short-term strength training was efficient in reducing this condition, regardless of body weight loss. In conclusion, there was a reduction of obesity-related hepatic lipogenesis and inflammation after short-term strength training, independent of weight loss, leading to improvements in hepatic insulin sensitivity and glycemic homeostasis in obese mice. Key points: (1) Short-term strength training (STST) reduced fat accumulation and inflammation in the liver; (2) Hepatic insulin sensitivity and HPG control were increased with STST; (3) The content and activity of ACC and content of FAS were reduced with STST; (4) STST improved hepatic fat accumulation and glycemic homeostasis; (5) STST effects were observed independently of body weight change.

scholarly journals Pregnancy facilitates maternal liver regeneration after partial hepatectomy

2020 ◽  
Vol 318 (4) ◽  
pp. G772-G780
Author(s):  
Joonyong Lee ◽  
Veronica Garcia ◽  
Shashank Manohar Nambiar ◽  
Huaizhou Jiang ◽  
Guoli Dai
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Liver Resection ◽  
Liver Regeneration ◽  
Partial Hepatectomy ◽  
Liver Fat ◽  
Fat Accumulation ◽  
Positive Effects ◽  
Maternal Liver ◽  
Hepatic Fat

Liver resection induces robust liver regrowth or regeneration to compensate for the lost tissue mass. In a clinical setting, pregnant women may need liver resection without terminating pregnancy in some cases. However, how pregnancy affects maternal liver regeneration remains elusive. We performed 70% partial hepatectomy (PH) in nonpregnant mice and gestation day 14 mice, and histologically and molecularly compared their liver regrowth during the next 4 days. We found that compared with the nonpregnant state, pregnancy altered the molecular programs driving hepatocyte replication, indicated by enhanced activities of epidermal growth factor receptor and STAT5A, reduced activities of cMet and p70S6K, decreased production of IL-6, TNFα, and hepatocyte growth factor, suppressed cyclin D1 expression, increased cyclin A1 expression, and early activated cyclin A2 expression. As a result, pregnancy allowed the remnant hepatocytes to enter the cell cycle at least 12 h earlier, increased hepatic fat accumulation, and enhanced hepatocyte mitosis. Consequently, pregnancy ameliorated maternal liver regeneration following PH. In addition, a report showed that maternal liver regrowth after PH is driven mainly by hepatocyte hypertrophy rather than hyperplasia during the second half of gestation in young adult mice. In contrast, we demonstrate that maternal liver relies mainly on hepatocyte hyperplasia instead of hypertrophy to restore the lost mass after PH. Overall, we demonstrate that pregnancy facilitates maternal liver regeneration likely via triggering an early onset of hepatocyte replication, accumulating excessive liver fat, and promoting hepatocyte mitosis. The results from our current studies enable us to gain more insights into how maternal liver regeneration progresses during gestation. NEW & NOTEWORTHY We demonstrate that pregnancy may generate positive effects on maternal liver regeneration following partial hepatectomy, which are manifested by early entry of the cell cycle of remnant hepatocytes, increased hepatic fat accumulation, enhanced hepatocyte mitosis, and overall accelerated liver regrowth.

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