scholarly journals Heterozygous deficiency of endoglin decreases insulin and hepatic triglyceride levels during high fat diet

2013 ◽  
Author(s):  
Daniel Beiroa ◽  
Romero-Pico Amparo ◽  
Langa Carmen ◽  
Bernabeu Carmelo ◽  
Lopez Miguel ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Hepatic Triglyceride ◽  
High Fat ◽  
Heterozygous Deficiency

scholarly journals Heterozygous Deficiency of Endoglin Decreases Insulin and Hepatic Triglyceride Levels during High Fat Diet

PLoS ONE ◽  
2013 ◽  
Vol 8 (1) ◽  
pp. e54591 ◽  
Author(s):  
Daniel Beiroa ◽  
Amparo Romero-Picó ◽  
Carmen Langa ◽  
Carmelo Bernabeu ◽  
Miguel López ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Hepatic Triglyceride ◽  
High Fat ◽  
Heterozygous Deficiency

scholarly journals FoxO3 regulates hepatic triglyceride metabolism via modulation of the expression of sterol regulatory-element binding protein 1c

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Liu Wang ◽  
Xiaopeng Zhu ◽  
Xiaoyang Sun ◽  
Xinyu Yang ◽  
Xinxia Chang ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Hepg2 Cells ◽  
Transcriptional Activity ◽  
Regulatory Element ◽  
Luciferase Reporter ◽  
Chow Diet ◽  
Hepatic Triglyceride ◽  
High Fat ◽  
Element Binding Protein ◽  
Sterol Regulatory Element

Abstract Background Excessive intrahepatic lipid accumulation is the major characteristic of nonalcoholic fatty liver disease (NAFLD). We sought to identify the mechanisms involved in hepatic triglyceride (TG) homeostasis. Forkhead box class O (FoxO) transcription factors have been shown to play an important role in hepatic metabolism. However, little is known about the effect of FoxO3 on hepatic TG metabolism. Methods Liver biopsy samples from patients with NALFD and liver tissues from high glucose and high sucrose (HFHS) fed mice, ob/ob mice and db/db mice were collected for protein and mRNA analysis. HepG2 cells were transfected with small interfering RNA to mediate FoxO3 knockdown, or adenovirus and plasmid to mediate FoxO3 overexpression. FoxO3-cDNA was delivered by adenovirus to the liver of C57BL/6 J male mice on a chow diet or on a high-fat diet, followed by determination of hepatic lipid metabolism. Sterol regulatory element-binding protein 1c (SREBP1c) luciferase reporter gene plasmid was co-transfected into HepG2 cells with FoxO3 overexpression plasmid. Results FoxO3 expression was increased in the livers of HFHS mice, ob/ob mice, db/db mice and patients with NAFLD. Knockdown of FoxO3 reduced whereas overexpression of FoxO3 increased cellular TG concentrations in HepG2 cells. FoxO3 gain-of-function caused hepatic TG deposition in C57BL/6 J mice on a chow diet and aggravated hepatic steatosis when fed a high-fat diet. Analysis of the transcripts established the increased expression of genes related to TG synthesis, including SREBP1c, SCD1, FAS, ACC1, GPAM and DGAT2 in mouse liver. Mechanistically, overexpression of FoxO3 stimulated the expression of SREBP1c, whereas knockdown of FoxO3 inhibited the expression of SREBP1c. Luciferase reporter assays showed that SREBP1c regulated the transcriptional activity of the SREBP1c promoter. Conclusions FoxO3 promotes the transcriptional activity of the SREBP1c promoter, thus leading to increased TG synthesis and hepatic TG accumulation.

scholarly journals Trans fat feeding results in higher serum alanine aminotransferase and increased insulin resistance compared with a standard murine high-fat diet

2009 ◽  
Vol 297 (2) ◽  
pp. G378-G384 ◽  
Author(s):  
Sean W. P. Koppe ◽  
Marc Elias ◽  
Richard H. Moseley ◽  
Richard M. Green
Keyword(s):  
Insulin Resistance ◽  
High Fat Diet ◽  
Trans Fat ◽  
Hepatic Triglyceride ◽  
High Fat ◽  
Trans Fats ◽  
Serum Alanine Aminotransferase ◽  
Triglyceride Content ◽  
In Trans ◽  
Fat Feeding

Diets high in trans fats are associated with an increased risk of cardiovascular disease and components of the metabolic syndrome. The influence of these toxic fatty acids on the development of nonalcoholic fatty liver disease has not been significantly examined. Therefore, we sought to compare the effect of a murine diet high in trans fat to a standard high-fat diet that is devoid of trans fats but high in saturated fats. Male AKR/J mice were fed a calorically identical trans fat diet or standard high-fat diet for 10 days, 4 wk, and 8 wk. Serum alanine aminotransferase (ALT), lipid, insulin, and leptin levels were determined and the quantitative insulin-sensitivity check index (QUICKI) was calculated as a measure of insulin resistance. Additionally, hepatic triglyceride content and gene expression of several proinflammatory genes were assessed. By 8 wk, trans fat-fed mice exhibited higher ALT values than standard high-fat-fed mice (126 ± 16 vs. 71 ± 7 U/l, P < 0.02) despite similar hepatic triglyceride content at each time point. Trans fat-fed mice also had increased insulin resistance compared with high-fat-fed mice at 4 and 8 wk with significantly higher insulin levels and lower QUICKI values. Additionally, hepatic interleukin-1β (IL-1β) gene expression was 3.6-fold higher at 4 wk ( P < 0.05) and 5-fold higher at 8 wk ( P < 0.05) in trans fat-fed mice compared with standard high-fat-fed mice. Trans fat feeding results in higher ALT values, increased insulin resistance, and elevated IL-1β levels compared with standard high-fat feeding.

scholarly journals CTRP3 attenuates diet-induced hepatic steatosis by regulating triglyceride metabolism

2013 ◽  
Vol 305 (3) ◽  
pp. G214-G224 ◽  
Author(s):  
Jonathan M. Peterson ◽  
Marcus M. Seldin ◽  
Zhikui Wei ◽  
Susan Aja ◽  
G. William Wong
Keyword(s):  
Lipid Metabolism ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Therapeutic Potential ◽  
Hepatic Triglyceride ◽  
Wild Type ◽  
High Fat ◽  
Triglyceride Synthesis ◽  
Modest Improvement ◽  
Protective Function

CTRP3 is a secreted plasma protein of the C1q family that helps regulate hepatic gluconeogenesis and is downregulated in a diet-induced obese state. However, the role of CTRP3 in regulating lipid metabolism has not been established. Here, we used a transgenic mouse model to address the potential function of CTRP3 in ameliorating high-fat diet-induced metabolic stress. Both transgenic and wild-type mice fed a high-fat diet showed similar body weight gain, food intake, and energy expenditure. Despite similar adiposity to wild-type mice upon diet-induced obesity (DIO), CTRP3 transgenic mice were strikingly resistant to the development of hepatic steatosis, had reduced serum TNF-α levels, and demonstrated a modest improvement in systemic insulin sensitivity. Additionally, reduced hepatic triglyceride levels were due to decreased expression of enzymes (GPAT, AGPAT, and DGAT) involved in triglyceride synthesis. Importantly, short-term daily administration of recombinant CTRP3 to DIO mice for 5 days was sufficient to improve the fatty liver phenotype, evident as reduced hepatic triglyceride content and expression of triglyceride synthesis genes. Consistent with a direct effect on liver cells, recombinant CTRP3 treatment reduced fatty acid synthesis and neutral lipid accumulation in cultured rat H4IIE hepatocytes. Together, these results establish a novel role for CTRP3 hormone in regulating hepatic lipid metabolism and highlight its protective function and therapeutic potential in attenuating hepatic steatosis.

Beet (Beta vulgaris L.) Stalk and Leaf Supplementation Improves Glucose Homeostasis and Insulin Resistance Markers in Liver of Mice Exposed to a High-Fat Diet

2020 ◽  
Author(s):  
Isabela Micheletti Lorizola ◽  
Josiane Érica Miyamoto ◽  
Ana Luiza Figueiredo Vieira ◽  
Beatriz Rocchetti Sumere ◽  
Rosângela Maria Neves Bezerra ◽  
...  
Keyword(s):  
Beta Vulgaris ◽  
Glucose Homeostasis ◽  
High Fat Diet ◽  
Standard Diet ◽  
Hepatic Triglyceride ◽  
High Fat ◽  
Treatment Groups ◽  
Triglyceride Content ◽  
Resistance Markers ◽  
Unhealthy Diet

Abstract Background Although beet stalks and leaves are not consumed and are usually discarded, they are an important source of bioactive flavonoids possessing antioxidant and anti-inflammatory activity, which could be explored to prevent metabolic disorders associated with an unhealthy diet. The aim of this study was to assess the effect of supplementation with beet (Beta vulgaris L.) stalks and leaves on metabolic parameters and glucose homeostasis in mice exposed to a high-fat diet.Methods Six-week-old male Swiss mice were randomly divided into five experimental groups submitted to either standard diet (CT) or high-fat diet (HF), and HF-fed mice were subdivided into three treatment groups supplemented with oven-dehydrated beet stalks and leaves (SL), lyophilized beet stalks and leaves (Ly) or beet stalk and leaf extract (EX).Results Supplementation with SL was able to ameliorate glucose homeostasis (P < 0.05) with no alteration in hepatic triglyceride content. It remains to be clarified if the enhancement in the glucose homeostasis observed in HFSL could be a consequence of improvement in pancreatic insulin secretion and/or glucose uptake from skeletal muscle and white adipose tissues.Conclusions The current results suggest that beet stalks and leaves could be used as adjuvants to improve parameters related to glucose metabolism in the liver.

scholarly journals Role of Synbiotics Containing d-Allulose in the Alteration of Body Fat and Hepatic Lipids in Diet-Induced Obese Mice

Nutrients ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 1797 ◽  
Author(s):  
Bo-Ra Choi ◽  
Eun-Young Kwon ◽  
Hye-Jin Kim ◽  
Myung-Sook Choi
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Food Industry ◽  
Lactobacillus Sakei ◽  
Obese Mice ◽  
Hepatic Triglyceride ◽  
High Fat ◽  
Hepatic Lipids ◽  
Diet Induced Obesity

The effects of allulose and two probiotic species on diet-induced obese (DIO) mice were investigated. Lactobacillus sakei LS03 (109 cfu/day) and Leuconostoc kimchii GJ2 (109 cfu/day) were used as probiotics, and allulose (AL) as a prebiotic. The synergistic effect of prebiotics and probiotics in improving obesity was evaluated. Orally fed Lactobacillus sakei LS03 (LS) or Leuconostoc kimchii GJ2 (GJ), significantly decreased hepatic triglyceride (TG) and fatty acid (FA) compared to the high-fat diet (HFD) control. AL markedly decreased visceral adiposity and pro-inflammatory adipokines (leptin and resistin) and cytokines (IL-6 and IL-1β) as well as hepatic TG and FA. In addition, AL exerted synergic effects with probiotics (LS and/or GJ) on the reduction of visceral white adipose tissue (WAT), associated with a decreased leptin: adiponectin ratio. There was no significant differences between the AL-SL and AL group, allulose and GJ combination (AL-GJ) was more effective than allulose in improving dyslipidemia, and decreasing WAT weight and hepatic FA, suggesting allulose may act as a favorable prebiotic for GJ supplement than LS. Combination of allulose with LS and GJ supplementation (AL-LSGJ) was the most effective for improving obesity related complications among the synbiotics groups containing allulose. In conclusion, this study demonstrated that the synbiotic mixture with allulose was more effective in suppressing diet-induced obese (DIO) and its complications via the regulation of lipid metabolism, than the probiotics or allulose alone, suggesting allulose may act as a prebiotic for the two probiotics tested in the study. This new synbiotic mixture with allulose may help ameliorate the deleterious effects of diet-induced obesity and contribute to the growth of the food industry.

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