Chlorogenic acid and caffeine in combination inhibit fat accumulation by regulating hepatic lipid metabolism-related enzymes in mice

Obesity has become a public health concern due to its positive association with the incidence of many diseases, and coffee components including chlorogenic acid (CGA) and caffeine have been demonstrated to play roles in the suppression of fat accumulation. To investigate the mechanism by which CGA and caffeine regulate lipid metabolism, in the present study, forty mice were randomly assigned to four groups and fed diets containing no CGA or caffeine, CGA, caffeine, or CGA+caffeine for 24 weeks. Body weight, intraperitoneal adipose tissue (IPAT) weight, and serum biochemical parameters were measured, and the activities and mRNA and protein expression of lipid metabolism-related enzymes were analysed. There was a decrease in the body weight and IPAT weight of mice fed the CGA+caffeine diet. There was a significant decrease in the serum and hepatic concentrations of total cholesterol, TAG and leptin of mice fed the CGA+caffeine diet. The activities of carnitine acyltransferase (CAT) and acyl-CoA oxidase (ACO) were increased in mice fed the caffeine and CGA+caffeine diets, while the activity of fatty acid synthase (FAS) was suppressed in those fed the CGA+caffeine diet. The mRNA expression levels of AMP-activated protein kinase (AMPK),CATandACOwere considerably up-regulated in mice fed the CGA+caffeine diet, while those ofPPARγ2were down-regulated. The protein expression levels of AMPK were increased and those of FAS were decreased in mice fed the CGA+caffeine diet. These results indicate that CGA+caffeine suppresses fat accumulation and body weight gain by regulating the activities and mRNA and protein expression levels of hepatic lipid metabolism-related enzymes and that these effects are stronger than those exerted by CGA and caffeine individually.

Download Full-text

Microcystin-LR altered mRNA and protein expression of endoplasmic reticulum stress signaling molecules related to hepatic lipid metabolism abnormalities in mice

Environmental Toxicology and Pharmacology ◽

10.1016/j.etap.2015.05.002 ◽

2015 ◽

Vol 40 (1) ◽

pp. 114-121 ◽

Cited By ~ 8

Author(s):

Wendi Qin ◽

Xuxiang Zhang ◽

Liuyan Yang ◽

Lizhi Xu ◽

Zongyao Zhang ◽

...

Keyword(s):

Endoplasmic Reticulum ◽

Lipid Metabolism ◽

Endoplasmic Reticulum Stress ◽

Protein Expression ◽

Signaling Molecules ◽

Stress Signaling ◽

Hepatic Lipid Metabolism ◽

Hepatic Lipid ◽

Mrna And Protein Expression

Download Full-text

Anti-Obesity Effects of Collagen Peptide Derived from Skate (Raja kenojei) Skin Through Regulation of Lipid Metabolism

Marine Drugs ◽

10.3390/md16090306 ◽

2018 ◽

Vol 16 (9) ◽

pp. 306 ◽

Cited By ~ 14

Author(s):

Minji Woo ◽

Yeong Song ◽

Keon-Hee Kang ◽

Jeong Noh

Keyword(s):

Body Weight ◽

Adipose Tissue ◽

Fatty Acid ◽

Lipid Metabolism ◽

Protein Expression ◽

The Body ◽

Chow Diet ◽

Dependent Manner ◽

Hepatic Lipid ◽

Collagen Peptide

This study investigated the anti-obesity effects of collagen peptide derived from skate skin on lipid metabolism in high-fat diet (HFD)-fed mice. All C57BL6/J male mice were fed a HFD with 60% kcal fat except for mice in the normal group which were fed a chow diet. The collagen-fed groups received collagen peptide (1050 Da) orally (100, 200, or 300 mg/kg body weight per day) by gavage, whereas the normal and control groups were given water (n = 9 per group). The body weight gain and visceral adipose tissue weight were lower in the collagen-fed groups than in the control group (p < 0.05). Plasma and hepatic lipid levels were significantly reduced by downregulating the hepatic protein expression levels for fatty acid synthesis (sterol regulatory element binding protein-1 (SREBP-1), fatty acid synthase (FAS), and acetyl-CoA carboxylase (ACC)) and cholesterol synthesis (SREBP-2 and 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR)) and upregulating those for β-oxidation (peroxisome proliferator-activated receptor alpha (PPAR-α) and carnitine palmitoyltransferase 1 (CPT1)) and synthesis of bile acid (cytochrome P450 family 7 subfamily A member 1 (CYP7A1)) (p < 0.05). In the collagen-fed groups, the hepatic protein expression level of phosphorylated 5′ adenosine monophosphate-activated protein kinase (p-AMPK) and plasma adiponectin levels were higher, and the leptin level was lower (p < 0.05). Histological analysis revealed that collagen treatment suppressed hepatic lipid accumulation and reduced the lipid droplet size in the adipose tissue. These effects were increased in a dose-dependent manner. The findings indicated that skate collagen peptide has anti-obesity effects through suppression of fat accumulation and regulation of lipid metabolism.

Download Full-text

Maternal high-fat diet consumption modulates hepatic lipid metabolism and microRNA-122 (miR-122) and microRNA-370 (miR-370) expression in offspring

British Journal Of Nutrition ◽

10.1017/s0007114514000579 ◽

2014 ◽

Vol 111 (12) ◽

pp. 2112-2122 ◽

Cited By ~ 79

Author(s):

R. O. Benatti ◽

A. M. Melo ◽

F. O. Borges ◽

L. M. Ignacio-Souza ◽

L. A. P. Simino ◽

...

Keyword(s):

Fatty Acid ◽

Lipid Metabolism ◽

High Fat Diet ◽

Fatty Acid Synthase ◽

High Fat ◽

Hepatic Lipid Metabolism ◽

Expression Levels ◽

Hepatic Lipid ◽

Pregnancy And Lactation ◽

Maternal Consumption

Maternal consumption of a high-fat diet (HFD) during pregnancy and lactation is closely related to hepatic lipid accumulation, insulin resistance and increased serum cytokine levels in offspring and into their adulthood. MicroRNA (miRNA) have been implicated in cholesterol biosynthesis and fatty acid metabolism. We evaluated the modulation of hepatic fatty acid synthesis (de novo), β-oxidation pathways, and miRNA-122 (miR-122) and miRNA-370 (miR-370) expression in recently weaned offspring (day 28) of mouse dams fed a HFD (HFD-O) or a standard chow (SC-O) during pregnancy and lactation. Compared with SC-O mice, HFD-O mice weighed more, had a larger adipose tissue mass and were more intolerant to glucose and insulin (P< 0·05). HFD-O mice also presented more levels of serum cholesterol, TAG, NEFA and hepatic IκB kinase and c-Jun N-terminal kinase phosphorylation compared with SC-O mice (P< 0·05). Protein levels of fatty acid synthase, acetyl-CoA carboxylase and 3-hydroxy-3-methylglutaryl-CoA reductase were similar in HFD-O and SC-O mice, whereas expression levels of SCD1 mRNA and protein were more abundant in HFD-O mice than in SC-O mice (P< 0·05). Interestingly, mRNA expression levels of the β-oxidation-related genes ACADVL and CPT1 were decreased in HFD-O mice (P< 0·05). Furthermore, the expression of miR-122 was reduced but that of miR-370 was increased in HFD-O mice compared with that in SC-O mice (P< 0·05). Changes in hepatic lipid metabolism were accompanied by increased mRNA content of AGPAT1 and TAG deposition in HFD-O mice (P< 0·05). Taken together, the present results strongly suggest that maternal consumption of a HFD affects the early lipid metabolism of offspring by modulating the expression of hepatic β-oxidation-related genes and miRNA that can contribute to metabolic disturbances in adult life.

Download Full-text

Influence of Genistein on Hepatic Lipid Metabolism in an In Vitro Model of Hepatic Steatosis

Molecules ◽

10.3390/molecules26041156 ◽

2021 ◽

Vol 26 (4) ◽

pp. 1156

Author(s):

Lena Seidemann ◽

Anne Krüger ◽

Victoria Kegel-Hübner ◽

Daniel Seehofer ◽

Georg Damm

Keyword(s):

Lipid Metabolism ◽

Liver Disease ◽

Protein Expression ◽

Hepatic Steatosis ◽

In Vitro Model ◽

Hepatic Lipid Metabolism ◽

Hepatic Lipid ◽

Genistein Treatment ◽

Vitro Model

Nonalcoholic fatty liver disease (NAFLD) is among the leading causes of end-stage liver disease. The impaired hepatic lipid metabolism in NAFLD is exhibited by dysregulated PPARα and SREBP-1c signaling pathways, which are central transcription factors associated with lipid degradation and de novo lipogenesis. Despite the growing prevalence of this disease, current pharmacological treatment options are unsatisfactory. Genistein, a soy isoflavone, has beneficial effects on lipid metabolism and may be a candidate for NAFLD treatment. In an in vitro model of hepatic steatosis, primary human hepatocytes (PHHs) were incubated with free fatty acids (FFAs) and different doses of genistein. Lipid accumulation and the cytotoxic effects of FFAs and genistein treatment were evaluated by colorimetric and enzymatic assays. Changes in lipid homeostasis were examined by RT-qPCR and Western blot analyses. PPARα protein expression was induced in steatotic PHHs, accompanied by an increase in CPT1L and ACSL1 mRNA. Genistein treatment increased PPARα protein expression only in control PHHs, while CPTL1 and ACSL1 were unchanged and PPARα mRNA was reduced. In steatotic PHHs, genistein reversed the increase in activated SREBP-1c protein. The model realistically reflected the molecular changes in hepatic steatosis. Genistein suppressed the activation of SREBP-1c in steatotic hepatocytes, but the genistein-mediated effects on PPARα were abolished by high hepatic lipid levels.

Download Full-text

Variation in genes related to hepatic lipid metabolism and changes in waist circumference and body weight

Genes & Nutrition ◽

10.1007/s12263-014-0385-7 ◽

2014 ◽

Vol 9 (2) ◽

Cited By ~ 2

Author(s):

Karina Meidtner ◽

Eva Fisher ◽

Lars Ängquist ◽

Claus Holst ◽

Karani S. Vimaleswaran ◽

...

Keyword(s):

Body Weight ◽

Lipid Metabolism ◽

Waist Circumference ◽

Hepatic Lipid Metabolism ◽

Hepatic Lipid

Download Full-text

Effects of Metformin Combined with Lactoferrin on Lipid Accumulation and Metabolism in Mice Fed with High-Fat Diet

Nutrients ◽

10.3390/nu10111628 ◽

2018 ◽

Vol 10 (11) ◽

pp. 1628 ◽

Cited By ~ 6

Author(s):

Qing-Qing Min ◽

Li-Qiang Qin ◽

Zhen-Zhen Sun ◽

Wen-Ting Zuo ◽

Lin Zhao ◽

...

Keyword(s):

Body Weight ◽

Lipid Metabolism ◽

Protein Expression ◽

Visceral Fat ◽

Lipid Accumulation ◽

High Fat Diet ◽

Control Group ◽

Lipolytic Enzyme ◽

High Fat ◽

Hepatic Lipid

Metformin (Met) and lactoferrin (Lf) both exhibit beneficial effects on body weight management and lipid accumulation. However, the synergistical action of Met and Lf remains unclear. In this study, 64 mice were divided into five groups, namely, the control group, high-fat diet (HFD group), HFD with Met (Met group), Lf (Lf group), and a combination of Met and Lf (Met + Lf group). Met (200 mg/kg body weight) and Lf (2 g/100 mL) were administrated in drinking water. The experiment lasted for 12 weeks. Body weight, serum, and hepatic lipids were determined. Histology of the liver and perirenal fat was observed. Protein expression related to hepatic lipid metabolism was also measured. HFD significantly increased body weight, visceral fat weight, and lipid profiles, which lead to obesity and dyslipidemia in mice. Compared with the HFD group, the treatments significantly decreased body weight and Lee’s index (body mass index of mice) with the lowest values in the Met + Lf group. The treatments also decreased the weight of visceral fat, and improved circulating lipid profile and the ability for regulating glucose intake. The adipocyte size and serum TC level were significantly lower in the Met + Lf group as compared with those in the Met or Lf group. The treatments alleviated hepatic lipid accumulation, especially in the Met + Lf group. For protein expression, the p-AMPK/AMPK ratio, a key kinase-regulating cellular energy homeostasis, was significantly higher in the Met + Lf group than the ratio in the HFD group. Similarly, the treatments significantly downregulated the protein expression of lipogenic enzymes (FAS, ACC, and SREBP-1) and upregulated the protein expression of lipolytic enzyme (ATGL). The protein expression of HMGCoAR, which is an important rate limiting enzyme in cholesterol biosynthesis, was only significantly lower in the Met + Lf group than in the HFD group. In conclusion, Met and Lf, either alone or in combination, prevented HFD-induced obesity and improved lipid metabolism.

Download Full-text