scholarly journals The Crude Extract fromPuerariaeFlower Exerts Antiobesity and Antifatty Liver Effects in High-Fat Diet-Induced Obese Mice

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Tomoyasu Kamiya ◽  
Mayu Sameshima-Kamiya ◽  
Rika Nagamine ◽  
Masahito Tsubata ◽  
Motoya Ikeguchi ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Uncoupling Protein ◽  
Expression Profiles ◽  
Folk Medicine ◽  
Hormone Sensitive Lipase ◽  
Leguminous Plant ◽  
Obese Mice ◽  
High Fat ◽  
Brown Adipose

Kudzu, a leguminous plant, has long been used in folk medicine. In particular, its flowers are used in Japanese and Chinese folk medicine for treating hangovers. We focused on the flower of Kudzu (Puerariae thomsonii), and we previously reported the antiobesity effect ofPuerariae thomsoniiflower extract (PFE) in humans. In this study, we conducted an animal study to investigate the effect of PFE on visceral fat and hepatic lipid levels in mice with diet-induced obesity. In addition, we focused on gene expression profiles to investigate the antiobesity mechanism of PFE. Male C57BL/6J mice were fed a high-fat diet (HFD) or an HFD supplemented with 5% PFE for 14 days. PFE supplementation significantly reduced body weight and white adipose tissue (WAT) weight. Moreover, in the histological analysis, PFE supplementation improved fatty liver. Hepatic reverse transcription-polymerase chain reaction revealed that PFE supplementation downregulated acetyl-CoA carboxylase expression. For adipose tissue, the expressions of hormone-sensitive lipase in WAT and uncoupling protein 1 in brown adipose tissue (BAT) were significantly upregulated. These results suggest that PFE exerts antiobesity and antifatty liver effects in high-fat diet-induced obese mice through suppressing lipogenesis in the liver, stimulating lipolysis in WAT, and promoting thermogenesis in BAT.

scholarly journals Deficiency of Cathelicidin Attenuates High-Fat Diet Plus Alcohol-Induced Liver Injury through FGF21/Adiponectin Regulation

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3333
Author(s):  
Fengyuan Li ◽  
Jenny Chen ◽  
Yunhuan Liu ◽  
Zelin Gu ◽  
Mengwei Jiang ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Alcohol Consumption ◽  
Liver Injury ◽  
High Fat Diet ◽  
Uncoupling Protein ◽  
Neutrophil Infiltration ◽  
Hormone Sensitive Lipase ◽  
Fibroblast Growth Factor 21 ◽  
High Fat ◽  
Brown Adipose

Alcohol consumption and obesity are known risk factors of steatohepatitis. Here, we report that the deficiency of CRAMP (cathelicidin-related antimicrobial peptide—gene name: Camp) is protective against a high-fat diet (HFD) plus acute alcohol (HFDE)-induced liver injury. HFDE markedly induced liver injury and steatosis in WT mice, which were attenuated in Camp–/– mice. Neutrophil infiltration was lessened in the liver of Camp–/– mice. HFDE feeding dramatically increased epididymal white adipose tissue (eWAT) mass and induced adipocyte hypertrophy in WT mice, whereas these effects were attenuated by the deletion of Camp. Furthermore, Camp–/– mice had significantly increased eWAT lipolysis, evidenced by up-regulated expression of lipolytic enzymes, adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL). The depletion of Camp also increased uncoupling protein 1 (UCP1)-dependent thermogenesis in the brown adipose tissue (BAT) of mice. HFDE fed Camp–/– mice had elevated protein levels of fibroblast growth factor 21 (FGF21) in the eWAT, with an increased adiponectin production, which had been shown to alleviate hepatic fat deposition and inflammation. Collectively, we have demonstrated that Camp–/– mice are protected against HFD plus alcohol-induced liver injury and steatosis through FGF21/adiponectin regulation. Targeting CRAMP could be an effective approach for prevention/treatment of high-fat diet plus alcohol consumption-induced steatohepatitis.

Thyroxine 5'-deiodinase in brown adipose tissue of myopathic hamsters

1986 ◽  
Vol 251 (1) ◽  
pp. E8-E13 ◽  
Author(s):  
J. Kopecky ◽  
L. Sigurdson ◽  
I. R. Park ◽  
J. Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
High Fat Diet ◽  
Uncoupling Protein ◽  
High Fat ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Uncoupling Protein ◽  
Endogenous Production ◽  
Deiodinase Activity ◽  
Brown Adipose

Myopathic Syrian hamsters (BIO 14.6) have less brown adipose tissue (BAT) than normal. The trophic response of this tissue to cold is smaller than normal and trophic responses to diet and to photoperiod are absent. The objective was to find out whether activity of thyroxine 5'-deiodinase in their BAT was increased normally in response to cold and thus whether a defect in endogenous production of 3,5,3'-triiodothyronine might underlie the attenuated trophic response. The effect of feeding a high-fat diet on activity of 5'-deiodinase was also studied. Cold acclimation increased thyroxine 5'-deiodinase activity in BAT of the myopathic hamster, but the total remained smaller than normal because of the smaller size. The cold-induced increase in concentration of mitochondrial uncoupling protein was also smaller than normal. The level of serum 3,5,3'-triiodothyronine was low in myopathic hamsters and remained lower than normal when they were cold-exposed or cold acclimated. Feeding the high-fat diet to myopathic hamsters resulted in a greater than normal suppression of thyroxine 5'-deiodinase activity than in normal hamsters; the normal increases in protein content and in concentration of mitochondrial uncoupling protein were absent. We conclude that the defective trophic response of BAT of the myopathic hamster is not secondary to defective regulation of its thyroxine 5'-deiodinase activity because this activity does not appear to be obligatorily linked to hypertrophy of BAT. The low level of serum 3,5,3'-triiodothyronine in the myopathic hamster may be secondary to reduced capacity for peripheral thyroxine deiodination in its BAT.

scholarly journals Crude Extracts fromLycium barbarumSuppress SREBP-1c Expression and Prevent Diet-Induced Fatty Liver through AMPK Activation

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Wang Li ◽  
Yan Li ◽  
Qing Wang ◽  
Yi Yang
Keyword(s):  
Fatty Liver ◽  
High Fat Diet ◽  
Uncoupling Protein ◽  
Expression Profiles ◽  
Liver Steatosis ◽  
High Fat ◽  
Lycium Barbarum ◽  
Brown Adipose

Lycium barbarumpolysaccharide (LBP) is well known in traditional Chinese herbal medicine that, has beneficial effects. Previous study reported that LBP reduced blood glucose and serum lipids. However, the underlying LBP-regulating mechanisms remain largely unknown. The main purpose of this study was to investigate whether LBP prevented fatty liver through activation of adenosine monophosphate-activated protein kinase (AMPK) and suppression of sterol regulatory element-binding protein-1c (SREBP-1c). Male C57BL/6J mice were fed a low-fat diet, high-fat diet, or 100 mg/kg LBP-treatment diet for 24 weeks. HepG2 cells were treated with LBP in the presence of palmitic acid. In our study, LBP can improve body compositions and lipid metabolic profiles in high-fat diet-fed mice. Oil Red O stainingin vivoandin vitroshowed that LBP significantly reduced hepatic intracellular triacylglycerol accumulation. H&E staining also showed that LBP can attenuate liver steatosis. Hepatic genes expression profiles demonstrated that LBP can activate the phosphorylation of AMPK, suppress nuclear expression of SREBP-1c, and decrease protein and mRNA expression of lipogenic genesin vivoorin vitro. Moreover, LBP significantly elevated uncoupling protein-1 (UCP1) and peroxisome proliferator-activated receptor-γcoactivator-1α(PGC-1α) expression of brown adipose tissue. In summary, LBP possesses a potential novel treatment in preventing diet-induced fatty liver.

scholarly journals Chronic Blockade of Nitric Oxide Synthesis Reduces Adiposity and Improves Insulin Resistance in High Fat-Induced Obese Mice

Endocrinology ◽  
2007 ◽  
Vol 148 (10) ◽  
pp. 4548-4556 ◽  
Author(s):  
Kyoichiro Tsuchiya ◽  
Haruna Sakai ◽  
Noriko Suzuki ◽  
Fumiko Iwashima ◽  
Takanobu Yoshimoto ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Uncoupling Protein ◽  
Serine Phosphorylation ◽  
Mrna Levels ◽  
Obese Mice ◽  
High Fat ◽  
Brown Adipose

Genetic deletion of inducible nitric oxide synthase (NOS) in mice has been shown to improve high-fat diet (HFD)-induced insulin resistance. However, a pathophysiological role of endogenous nitric oxide (NO) in obesity-related insulin resistance remains controversial. To address this issue, we examined the metabolic phenotypes in HFD-induced obese mice with chronic blockade of NO synthesis by a NOS inhibitor, N(G)-nitro-l-arginine methyl ester (L-NAME). Six-week-old male C57BL/6j mice were provided free access to either a standard diet (SD) or a HFD and tap water with or without L-NAME (100 mg/kg·d) for 12 wk. L-NAME treatment significantly attenuated body weight gain of mice fed either SD or HFD without affecting calorie intake. L-NAME treatment in HFD-fed mice improved glucose tolerance and insulin sensitivity. HFD feeding induced inducible NOS mRNA expression, but not the other two NOS isoforms, in white adipose tissue (WAT) and skeletal muscle. L-NAME treatment up-regulated uncoupling protein-1 in brown adipose tissue of HFD-fed mice but down-regulated monocyte chemoattractant protein-1 and CD68 mRNAs levels in WAT. HFD feeding up-regulated leptin mRNA levels but conversely down-regulated adiponectin mRNA levels in WAT, but these effects were unaffected by L-NAME treatment. Moreover, L-NAME treatment also increased peroxisome proliferator-uncoupling protein-3 mRNA levels in skeletal muscles of HFD-fed mice. Increased urinary excretion of norepinephrine after HFD feeding was augmented in L-NAME-treated mice. Insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 and serine phosphorylation of Akt/Akt2 in soleus muscle was markedly impaired in HFD-fed mice but reversed by L-NAME treatment. In conclusion, chronic NOS blockade by L-NAME in mice ameliorates HFD-induced adiposity and glucose intolerance, accompanied by reduced adipose inflammation and improved insulin signaling in skeletal muscle, suggesting that endogenous NO plays a modulatory role in the development of obesity-related insulin resistance.

The treatment with an extract from Calafate (Berberis microphylla) induces transcript and protein expression of molecules involved in thermogenesis and adipocyte browning in adipose tissue from obese mice

2021 ◽  
pp. 1-11
Author(s):  
Lissette Duarte ◽  
Javier Quezada ◽  
Luisa A. Ramirez ◽  
Karla Vasquez ◽  
Juan F. Orellana ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Control Diet ◽  
Obese Mice ◽  
High Fat ◽  
Total Polyphenols ◽  
Adipose Tissues ◽  
Protein Levels ◽  
Brown Adipose ◽  
Diet Control

BACKGROUND: Polyphenols intake increases the function of brown adipose tissue (BAT), stimulating energy expenditure (EE). Calafate (Berberis microphylla) is a polyphenol-rich Chilean native fruit. OBJECTIVE: To analyse the effect of a treatment with a Calafate extract in the thermogenic activity of mice adipose tissues. METHODS: Forty adult C57BL/6J male mice were subdivided into four groups (n=10 each): control diet, control+Calafate (extract: 50mg total polyphenols/kg weight), high-fat diet (HF) and HF+Calafate. RESULTS: Calafate prevented the increase in body weight and the decrease EE induced by HF. In BAT, Ucp-1 transcript was influenced by the interaction between diet and Calafate (p<0.01), Pparα showed the same expression pattern as Ucp-1 and both, diet (p<0.01) and Calafate (p<0.05), induced significant effects in Sirt1. In inguinal adipose tissue, Pgc1α, Pparα, Prdm16, Sirt1, and Dio2 transcripts presented a decreased expression caused by HF, that was reversed by Calafate. In BAT, an effect of diet (p<0.05) and an interaction between diet and Calafate (p<0.01) was observed in UCP-1 protein levels. CONCLUSIONS: A treatment with Calafate drives less weight gain in mice fed with HF, and reverses the effects generated by it on the expression of thermogenic and browning markers.

Defective adaptive thermogenesis contributes to metabolic syndrome and liver steatosis in obese mice

2017 ◽  
Vol 131 (4) ◽  
pp. 285-296 ◽  
Author(s):  
Laurence Poekes ◽  
Vanessa Legry ◽  
Olivier Schakman ◽  
Christine Detrembleur ◽  
Anne Bol ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Cold Exposure ◽  
High Fat Diet ◽  
Liver Steatosis ◽  
Obese Mice ◽  
High Fat ◽  
Adaptive Thermogenesis ◽  
Brown Adipose ◽  
Sympathetic Pathway

Defective adaptive high-fat diet (HFD)- and cold-induced thermogenesis, due to impaired sympathetic pathway in brown adipose tissue (BAT), contribute to metabolic syndrome and fatty liver. Improving thermogenic capacities by repeated cold exposure alleviates metabolic and hepatic complications of obesity.

scholarly journals Pathological Conversion of Mouse Perivascular Adipose Tissue by Notch Activation

2020 ◽  
Vol 40 (9) ◽  
pp. 2227-2243 ◽  
Author(s):  
Joshua M. Boucher ◽  
Larisa Ryzhova ◽  
Anne Harrington ◽  
Jessica Davis-Knowlton ◽  
Jacqueline E. Turner ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Notch Signaling ◽  
High Fat Diet ◽  
Vascular Function ◽  
Uncoupling Protein ◽  
Standard Diet ◽  
Lipid Deposition ◽  
High Fat ◽  
Perivascular Adipose Tissue ◽  
Brown Adipose

Objective: Perivascular adipose tissue (PVAT) surrounding arteries supports healthy vascular function. During obesity, PVAT loses its vasoprotective effect. We study pathological conversion of PVAT, which involves molecular changes in protein profiles and functional changes in adipocytes. Approach and Results: C57BL6/J mice were fed a 60% high-fat diet for 12 weeks or a cardioprotective 30% calorie-restricted diet for 5 weeks. Proteomic analysis identified PVAT as a molecularly distinct adipose depot, and novel markers for thermogenic adipocytes, such as GRP75 (stress-70 protein, mitochondrial), were identified. High-fat diet increased the similarity of protein signatures in PVAT and brown adipose, suggesting activation of a conserved whitening pathway. The whitening phenotype was characterized by suppression of UCP1 (uncoupling protein 1) and increased lipid deposition, leptin, and inflammation, and specifically in PVAT, elevated Notch signaling. Conversely, PVAT from calorie-restricted mice had decreased Notch signaling and less lipid. Using the Adipoq-Cre strain, we constitutively activated Notch1 signaling in adipocytes, which phenocopied the changes in PVAT caused by a high-fat diet, even on a standard diet. Preadipocytes from mouse PVAT expressed Sca1, CD140a, Notch1, and Notch2, but not CD105, showing differences compared with preadipocytes from other depots. Inhibition of Notch signaling during differentiation of PVAT-derived preadipocytes reduced lipid deposition and adipocyte marker expression. Conclusions: PVAT shares features with other adipose depots, but has a unique protein signature that is regulated by dietary stress. Increased Notch signaling in PVAT is sufficient to initiate the pathological conversion of PVAT by promoting adipogenesis and lipid accumulation and may thus prime the microenvironment for vascular disease.

scholarly journals Cranberry Polyphenolic Extract Exhibits an Antiobesity Effect on High-Fat Diet–Fed Mice through Increased Thermogenesis

2020 ◽  
Vol 150 (8) ◽  
pp. 2131-2138 ◽  
Author(s):  
Fang Zhou ◽  
Jielong Guo ◽  
Xue Han ◽  
Yunxiao Gao ◽  
Qimin Chen ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Uncoupling Protein ◽  
The Body ◽  
High Fat ◽  
Uncoupling Protein 1 ◽  
Polyphenolic Extract ◽  
Brown Adipose

ABSTRACT Background Although polyphenol-rich cranberry extracts reportedly have an antiobesity effect, the exact reason for this remains unclear. Objectives In light of the reported health benefits of the polyphenolic compounds in cranberry, we investigated the effects and mechanism of a cranberry polyphenolic extract (CPE) in high-fat diet (HFD)–fed obese mice. Methods The distributions of individual CPE compounds were characterized by HPLC fingerprinting. Male C57BL/6J mice (4 wk old) were fed for 16 wk normal diet (ND, 10% fat energy) or HFD (60% fat energy) with or without 0.75% CPE in drinking water (HFD + CPE). Body and adipose depot weights, indices of glucose metabolism, energy expenditure (EE), and expression of genes related to brown adipose tissue (BAT) thermogenesis, and inguinal/epididymal white adipose tissue (iWAT/eWAT) browning were measured. Results After 16 wk, the body weight was 22.5% lower in the CPE-treated mice than in the HFD group but remained 17.9% higher than in the ND group. CPE treatment significantly increased EE compared with that of the ND and HFD groups. The elevated EE was linked with BAT thermogenesis, and iWAT/eWAT browning, shown by the induction of thermogenic genes, especially uncoupling protein 1 (Ucp1), and browning-related genes, including Cd137, a member of the tumor necrosis factor receptor superfamily (Tnfrsf9). The mRNA expression and abundance of uncoupling protein 1 in BAT of CPE-fed mice were 5.78 and 1.47 times higher than in the HFD group, and 0.61 and 1.12 times higher than in the ND group, respectively. Cd137 gene expression in iWAT and eWAT of CPE-fed mice were 2.35 and 3.13 times higher than in the HFD group, and 0.84 and 1.39 times higher than in the ND group, respectively. Conclusions Dietary CPE reduced but did not normalize HFD-induced body weight gain in male C57BL/6J mice, possibly by affecting energy metabolism.

Control of norepinephrine turnover in brown adipose tissue of Syrian hamsters

1988 ◽  
Vol 254 (6) ◽  
pp. R960-R968
Author(s):  
S. L. Sigurdson ◽  
J. Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
High Fat Diet ◽  
Uncoupling Protein ◽  
Short Photoperiod ◽  
High Fat ◽  
Syrian Hamsters ◽  
Norepinephrine Turnover ◽  
Low T3 ◽  
Brown Adipose

Sympathetic nervous system activity in brown adipose tissue (BAT) of normal and myopathic Syrian hamsters was assessed by measuring norepinephrine turnover rate (NETR) using [3H]norepinephrine. Acute exposure of normal hamsters to cold (4 degrees C) for 4 or 24 h increased norepinephrine secretion but not resynthesis. By 3 days and at 2 wk in the cold, NETR increased but returned to a normal level by 6 wk. Hamsters were initially hypothermic (to 3 days) then normothermic (2 and 6 wk). Adaptation of normal or myopathic hamsters to high-fat diet or short photoperiod (4 h light, 20 h dark) for up to 12 wk did not alter NETR in BAT. Serum triiodothyronine (T3) concentration increased rapidly in the cold to reach a maximum level by 24 h at which it remained for 6 wk and was not correlated with changes in NETR in BAT. The high-fat diet did not alter T3 level in normal hamsters; it increased the low T3 level in myopathic hamsters. Short photoperiod induced a transient increase in T3 level in normal hamsters but not in myopathic hamsters. We conclude that the hypertrophied state of BAT in Syrian hamsters adapted to cold, to high-fat diet, or to short photoperiod is not maintained by elevated norepinephrine secretion and that some other factor(s) must be involved. A selective increase in concentration of BAT mitochondrial uncoupling protein in hamsters may be dependent on raised T3 level in serum and/or production in BAT, since both occur in response to cold acclimation but not in response to high-fat diet or short photoperiod.

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