scholarly journals Effect of microencapsulated Lactobacillus plantarum LIP-1 on cholesterol metabolism in hyperlipidaemic rats

2019 ◽  
Author(s):  
Caiqing Yao ◽  
Wenjing Tian ◽  
Jiaojiao Song ◽  
Junguo Wang
Keyword(s):  
Lipid Metabolism ◽  
Lactobacillus Plantarum ◽  
High Fat Diet ◽  
Cholesterol Metabolism ◽  
Normal Diet ◽  
Hypolipidemic Effect ◽  
High Fat ◽  
Prevention And Cure

Abstract Background: Previous studies have shown that Lactobacillus plantarum LIP-1 has obvious hypolipidemic effect, and microencapsulated probiotics can ensure the strains live through the gastrointestinal tract, although there has been much research on both preparation and assessment methods for probiotics microcapsules, most assessments are made in vitro and few are validated in vivo. In this study, the protective effect of microencapsulation and the possible hypolipidaemic mechanisms of probiotic Lactobacillus plantarum LIP-1 (hereafter LIP-1) were evaluated in rats. Methods: Treatments included rats fed on: normal diet, high-fat diet, high-fat diet with an intragastric supplement of either non-microencapsulated LIP-1 cells (NME LIP-1) or microencapsulated LIP-1 (ME LIP-1). Lipid metabolism indicators were measured during the experiment and following euthanasia. Results: Microencapsulation increased survival and colonization of LIP-1 in the colon. ME LIP-1 was superior to NME LIP-1 in reducing cholesterol. The mechanisms behind the hypolipidemic effect exerted by LIP-1 are possibly due to: promoting the excretion of cholesterol, improving antioxygenic potentials, enhancing recovery from the injury in the liver and intestinal mucosa, promoting the generation of SCFAs, and improving lipid metabolism. Conclusions: This study confirms the role of ME LIP-1 in the prevention and cure of hyperlipidemia and provides theoretical support for the probiotics to enter clinical use. Keywords: Microencapsulated LIP-1; non-microencapsulated LIP-1 cells; hypolipidaemic effect; lipid metabolism; antioxidative activity

scholarly journals Hepatic Lipid Accumulation Induced by a High-fat Diet Is Regulated by Nrf2 Through Multiple Pathways

2021 ◽  
Author(s):  
sheng Qiu ◽  
Zerong Liang ◽  
Qinan Wu ◽  
Miao Wang ◽  
Mengliu Yang ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Underlying Mechanism ◽  
Luciferase Assay ◽  
High Fat ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation

Abstract BackgroundNuclear factor erythroid 2-related factor 2 (Nrf2) is reportedly involved in hepatic lipid metabolism, but the results are contradictory and the underlying mechanism thus remains unclear. Herein we focused on elucidating the effects of Nrf2 on hepatic adipogenesis and on determining the possible underlying mechanism. We established a metabolic associated fatty liver disease (MAFLD) model in high fat diet (HFD) fed Nrf2 knockout (Nrf2 KO) mice; further, a cell model of lipid accumulation was established using mouse primary hepatocytes (MPHs) treated with free fatty acids (FAs). Using these models, we investigated the relationship between Nrf2 and autophagy and its role in the development of MAFLD.ResultsWe observed that Nrf2 expression levels were up-regulated in patients with MAFLD and diet-induced obese mice. Nrf2 deficiency led to hepatic lipid accumulation in vivo and in vitro, in addition to, promoting lipogenesis mainly by increasing SREBP-1 activity. Moreover, Nrf2 deficiency attenuated autophagic flux and inhibited the fusion of autophagosomes and lysosomes in vivo and in vitro. Weakened autophagy caused reduced lipolysis in the liver. Importantly, Chromatin immunoprecipitation-qPCR (ChIP-qPCR) and dual-luciferase assay results proved that Nrf2 bound to LAMP1 promoter and regulated its transcriptional activity. We accordingly report that Nrf2-LAMP1 interaction has an indispensable role in Nrf2-regulated hepatosteatosis. ConclusionsThese data collectively confirm that Nrf2 deficiency promotes hepatosteatosis by enhancing SREBP-1 activity and attenuating autophagy. To conclude, our data reveal a novel multi-pathway effect of Nrf2 on lipid metabolism in the liver, and we believe that multi-target intervention of Nrf2 signaling is a promising new strategy for the prevention and treatment of MAFLD.

Effects of Hwangryunjihwang-tang on In Vitro Fertilization and Ovulation in Mice Fed a High-fat Diet

2003 ◽  
Vol 31 (02) ◽  
pp. 213-223
Author(s):  
H. G. Choi ◽  
D. H. Kwak ◽  
J. Y. Kim ◽  
Y. J. Choi ◽  
B. S. Kil ◽  
...  
Keyword(s):  
Body Weight ◽  
Embryonic Development ◽  
High Fat Diet ◽  
Normal Diet ◽  
The Body ◽  
High Fat ◽  
Reproductive Dysfunction ◽  
Vitro Fertilization

It has been generally accepted that Hwangryunjihwang-tang (H-tang) is a useful prescription for treating polydipsia and to prevent obesity induced by a high-fat diet. The aim of this study was to clarify whether H-tang improved reproductive dysfunction caused by obesity in mice. Mice were fed a high density protein and lipid diet for 4 weeks, followed by administration of H-tang at 480 mg/kg body weight per day for 4 days. Thereafter, changes of body weight, ovulation rate, in vitro and in vivo fertilization, embryonic development and implantation rate were measured. H-tang markedly reduced the body weight of obese mice fed a high-fat diet, but not mice fed a normal diet. H-tang significantly improved ovulation rates, in vitro and in vivo fertilization rates and embryonic development. These results indicate pharmacological reversal of reproductive dysfunction caused by obesity, perhaps by adjusting internal secretions and metabolic functions.

scholarly journals The PCSK9 Involves in the Dyslipidemia of Ovariectomized Mice and Its Mechanism

2021 ◽  
Author(s):  
Dan Zhao ◽  
Xue-qin Zhang ◽  
Wen-jing Guo ◽  
Zhi-hui Cui ◽  
Yi-cheng Wang ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
High Fat Diet ◽  
Cholesterol Metabolism ◽  
Critical Role ◽  
Normal Diet ◽  
High Fat ◽  
Lipid Metabolism Disorder ◽  
Pcsk9 Inhibitor ◽  
Metabolism Disorder ◽  
Ovariectomized Mice

Abstract Ovarian failure in postmenopausal female leads E2 to dramatic decrease which is an important reason of menopausal dyslipidemia. PCSK9 as a secretory lipid metabolic regulator plays a critical role in the cholesterol metabolism by negatively regulating LDLR in hepatocytes. Clinical data showed PCSK9 was elevated and positively correlated with LDL-C in the blood of postmenopausal women. However, the relationship between E2 and PCSK9 and the role of PCSK9 in postmenopausal dyslipidemia are still unclear. In this research, 10-week-old ovariectomized mice were fed for 4 weeks with normal diet or high-fat diet, then tested the lipid metabolism profiles and PCSK9 in the blood and the expression of LDLR and PCSK9 in the liver. On this basis, PCSK9-/- ovariectomized mice were used to further verify the effect of PCSK9 in dyslipidemia of ovariectomized mice. Finally, the ovariectomized mice with high-fat diet were subcutaneous injected respectively with E2 or PCSK9 inhibitor alone or both together for 2 weeks and were tested as previous experiment. The results showed PCSK9, TC and LDL-c all increased in the blood of in WT ovariectomized mice and their PCSK9 is positively correlated with LDL-c, while there were on obvious lipid metabolism disorder in the PCSK9−/− ovariectomized mice. PCSK9 inhibitor increased the LDLR on the liver and ameliorated the dyslipidemia in WT ovariectomized mice. It suggests that PCSK9 plays an important role in the dyslipidemia of ovariectomized mice, which provides a new strategy for clinical diagnosis and treatment of the dyslipidemia in post-menopause.

scholarly journals Antihyperlipidemic activity of newly synthesized piperlonguminine acid

2018 ◽  
Vol 25 (03) ◽  
pp. 97-105
Author(s):  
Mungunnaran D ◽  
Gereltu B ◽  
Bayarmaa B
Keyword(s):  
Molecular Structure ◽  
Lipid Metabolism ◽  
Oral Administration ◽  
1H Nmr ◽  
High Fat Diet ◽  
Hypolipidemic Effect ◽  
High Fat ◽  
Piper Longum ◽  
Antihyperlipidemic Activity

Abnormalities in lipid metabolism cause many diseases, including atherosclerosis. By this study, we proposed to synthesize a novel derivative from piperine and identify its hypolipidemic effect. For this, piperlonguminine acid (GBN-COOH) was synthesized as a piperine derivative from Piper longum Linn. successfully. The molecular structure of the GBN-COOH was confirmed by 13C and 1H NMR, ES-MS methods and it was administered orally to high-fat diet fed rats. Compared with model rats, oral administration of GB-COOH at dose of 10 mg/kg to hyperlipidemic rats could significantly decrease the levels of serum TC, TG, and LDL-C by the amount of 4.93 mm/L, 1.15 mm/L, and 1.11 mm/L, respectively, with increase of HDL-C level from 0.19 mm/L to 0.26 mm/L. Thus, the synthesized piperlonguminine acid could be a useful candidate in the treatment of anti-hyperlipidemia. Шинээр гарган авсан пиперлонгуминины хүчлийн өөх-тосны эсрэг идэвхийн судалгаа Хураангуй:  Өөх-тосны солилцооны эмгэгийн үед судасны хатуурал буюу атеросклероз өвчин үүсдэг бөгөөд энэ үед өндөр нягттай липопротейдын цусанд агуулагдах хэмжээ буурч, бага нягттай липопротеины хэмжээ өсдөг. Бид энэхүү судалгаагаар цусан дахь өөх-тосны хэмжээг бууруулах идэвхтэй шинэ нэгдлийг гарган авах зорилгоор хүнс болон уламжлалт анагаах ухаанд өргөн ашигладаг хар чинжүү буюу бивлэн (Piper longum)-ийн пиперин алкалоидоос пиперлонгуминины хүчлийг нийлэгжүүлэн гарган авч, өөх-тосны солилцоонд үйлчлэх үйлдлийг in vivo нөхцөлд туршилтын хулгана дээр судлав. Судалгааны дүнд шинээр нийлэгжүүлэн гарган авсан пиперлонгуминины хүчил нийт холестерин, триглицерид, бага нягттай липопротеины хэмжээг 4.93 мм/л, 1.15 мм/л, 1.11 мм/л хэмжээгээр тус тус бууруулж, их нягттай липопротеины хэмжээг 0.19 мм/л-ээс 0.26 мм/л болтол өсгөж байгаа нь цусан дахь өөх-тосны хэмжээг бууруулах өндөр идэвхтэй болох ба судас хатуурах өвчнөөс урьдчилан сэргийлэх бэлдмэл болгон ашиглах боломжтойг харуулж байна. Түлхүүр үг: Пиперин, Piper longum, холестерин, атеросклероз, нийлэгжүүлэлт

scholarly journals Targeting of adipose tissue macrophages by bee venom phospholipase A2 attenuates high-fat diet-induced obesity

2021 ◽  
Author(s):  
Hyunju Jeong ◽  
Chanju Lee ◽  
Chenyu Cheng ◽  
Hung Chun Chou ◽  
HyeJin Yang ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Phospholipase A2 ◽  
High Fat Diet ◽  
Normal Diet ◽  
Bee Venom ◽  
High Fat ◽  
Adipose Tissue Macrophages ◽  
Anti Inflammatory

Abstract Background/objectives Adipose tissue macrophages (ATMs) exist in either the M1 or M2 form. The anti-inflammatory M2 ATMs accumulate in lean individuals, whereas the pro-inflammatory M1 ATMs accumulate in obese individuals. Bee venom phospholipase A2 (bvPLA2), a major component in honeybee (Apis mellifera) venom, exerts potent anti-inflammatory effects via interactions with regulatory T cells (Treg) and macrophages. This study investigated the effects of bvPLA2 on a high-fat diet (HFD)-induced obesity in mice. Subjects/methods For in vivo experiments, male C57BL/6, CD206-deficient, and Treg-depleted mice models were fed either a normal diet 41.86 kJ (ND, 10 kcal% fat) or high-fat diet 251.16 kJ (HFD, 60 kcal% fat). Each group was i.p. injected with PBS or bvPLA2 (0.5 mg/kg) every 3 days for 11 weeks. Body weight and food intake were measured weekly. Histological changes in the white adipose tissue (WAT), liver, and kidney as well as the immune phenotypes of the WAT were examined. Immune cells, cytokines, and lipid profiles were also evaluated. The direct effects of bvPLA2 on 3T3-L1 pre-adipocytes and bone marrow-derived macrophages were measured in vitro. Results bvPLA2 markedly decreased bodyweight in HFD-fed mice. bvPLA2 treatment also decreased lipid accumulation in the liver and reduced kidney inflammation in the mice. It was confirmed that bvPLA2 exerted immunomodulatory effects through the CD206 receptor. In addition, bvPLA2 decreased M1 ATM and alleviated the M1/M2 imbalance in vivo. However, bvPLA2 did not directly inhibit adipogenesis in the 3T3-L1 adipose cells in vitro. Conclusions bvPLA2 is a potential therapeutic strategy for the management of obesity by regulating adipose tissue macrophage homeostasis.

scholarly journals Liver-Specific Overexpression of Prostasin Attenuates High-Fat Diet-Induced Metabolic Dysregulation in Mice

2021 ◽  
Vol 22 (15) ◽  
pp. 8314
Author(s):  
Tetsuo Sekine ◽  
Soichi Takizawa ◽  
Kohei Uchimura ◽  
Asako Miyazaki ◽  
Kyoichiro Tsuchiya
Keyword(s):  
Lipid Metabolism ◽  
High Fat Diet ◽  
Intima Media Thickness ◽  
High Fat ◽  
Glucose And Lipid Metabolism ◽  
Extracellular Signal ◽  
Hepatic Fat ◽  
Kinase Phosphorylation

The liver has a most indispensable role in glucose and lipid metabolism where we see some of the most serious worldwide health problems. The serine protease prostasin (PRSS8) cleaves toll-like receptor 4 (TLR4) and regulates hepatic insulin sensitivity under PRSS8 knockout condition. However, liver substrate proteins of PRSS8 other than TLR4 and the effect to glucose and lipid metabolism remain unclarified with hepatic elevation of PRSS8 expression. Here we show that high-fat-diet-fed liver-specific PRSS8 transgenic mice improved glucose tolerance and hepatic steatosis independent of body weight. PRSS8 amplified extracellular signal-regulated kinase phosphorylation associated with matrix metalloproteinase 14 activation in vivo and in vitro. Moreover, in humans, serum PRSS8 levels reduced more in type 2 diabetes mellitus (T2DM) patients than healthy controls and were lower in T2DM patients with increased maximum carotid artery intima media thickness (>1.1 mm). These results identify the regulatory mechanisms of PRSS8 overexpression over glucose and lipid metabolism, as well as excessive hepatic fat storage.

scholarly journals Adipocyte-specific deletion of Tcf7l2 induces dysregulated lipid metabolism and impairs glucose tolerance in mice

Diabetologia ◽  
2020 ◽  
Vol 64 (1) ◽  
pp. 129-141
Author(s):  
Marie-Sophie Nguyen-Tu ◽  
Aida Martinez-Sanchez ◽  
Isabelle Leclerc ◽  
Guy A. Rutter ◽  
Gabriela da Silva Xavier
Keyword(s):  
Insulin Secretion ◽  
Lipid Metabolism ◽  
Glucose Tolerance ◽  
High Fat Diet ◽  
Diabetes Risk ◽  
High Fat ◽  
Normal Chow ◽  
Glucose Stimulated Insulin Secretion

Abstract Aims/hypothesis Transcription factor 7-like 2 (TCF7L2) is a downstream effector of the Wnt/β-catenin signalling pathway implicated in type 2 diabetes risk through genome-wide association studies. Although its expression is critical for adipocyte development, the potential roles of changes in adipose tissue TCF7L2 levels in diabetes risk are poorly defined. Here, we investigated whether forced changes in Tcf7l2 expression in adipocytes affect whole body glucose or lipid metabolism and crosstalk between disease-relevant tissues. Methods Tcf7l2 was selectively ablated in mature adipocytes in C57BL/6J mice using Cre recombinase under Adipoq promoter control to recombine Tcf7l2 alleles floxed at exon 1 (referred to as aTCF7L2 mice). aTCF7L2 mice were fed normal chow or a high-fat diet for 12 weeks. Glucose and insulin sensitivity, as well as beta cell function, were assessed in vivo and in vitro. Levels of circulating NEFA, selected hormones and adipokines were measured using standard assays. Results Reduced TCF7L2 expression in adipocytes altered glucose tolerance and insulin secretion in male but not in female mice. Thus, on a normal chow diet, male heterozygote knockout mice (aTCF7L2het) exhibited impaired glucose tolerance at 16 weeks (p = 0.03) and increased fat mass (1.4 ± 0.1-fold, p = 0.007) but no changes in insulin secretion. In contrast, male homozygote knockout (aTCF7L2hom) mice displayed normal body weight but impaired oral glucose tolerance at 16 weeks (p = 0.0001). These changes were mechanistically associated with impaired in vitro glucose-stimulated insulin secretion (decreased 0.5 ± 0.1-fold vs control mice, p = 0.02) and decreased levels of the incretins glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide (0.6 ± 0.1-fold and 0.4 ± 0.1-fold vs control mice, p = 0.04 and p < 0.0001, respectively). Circulating levels of plasma NEFA and fatty acid binding protein 4 were increased by 1.3 ± 0.1-fold and 1.8 ± 0.3-fold vs control mice (p = 0.03 and p = 0.05, respectively). Following exposure to a high-fat diet for 12 weeks, male aTCF7L2hom mice exhibited reduced in vivo glucose-stimulated insulin secretion (0.5 ± 0.1-fold vs control mice, p = 0.02). Conclusions/interpretation Loss of Tcf7l2 gene expression selectively in adipocytes leads to a sexually dimorphic phenotype, with impairments not only in adipocytes, but also in pancreatic islet and enteroendocrine cells in male mice only. Our findings suggest novel roles for adipokines and incretins in the effects of diabetes-associated variants in TCF7L2, and further illuminate the roles of TCF7L2 in glucose homeostasis and diabetes risk.

HGF ameliorates a high-fat diet-induced fatty liver

2007 ◽  
Vol 293 (1) ◽  
pp. G204-G210 ◽  
Author(s):  
Takashi Kosone ◽  
Hitoshi Takagi ◽  
Norio Horiguchi ◽  
Yasuyo Ariyama ◽  
Toshiyuki Otsuka ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Fatty Liver ◽  
Cell Line ◽  
Hepg2 Cell ◽  
High Fat Diet ◽  
Normal Diet ◽  
Hepg2 Cell Line ◽  
High Fat

Hepatocyte growth factor (HGF) has various effects especially on epithelial cells. However, the precise role of HGF on lipogenesis is still not fully understood. A high-fat diet was administered to HGF transgenic mice and wild-type control mice in vivo. Furthermore, recombinant human HGF (rhHGF) was administered to HepG2 cell line in vitro. We performed an analysis regarding the factors relating to lipid metabolism. An overexpression of HGF dramatically ameliorates a high-fat diet-induced fatty liver. HGF transgenic mice showed an apparently reduced lipid accumulation in the liver. The activation of microsomal triglyceride transfer protein (MTP) and apolipoprotein B (ApoB) accompanying higher triglyceride levels in the serum were found in HGF transgenic mice on a normal diet. Interestingly, this upregulation of the MTP activation became more apparent in the high-fat diet. In addition, the administration of rhHGF stimulated MTP and ApoB expression while reducing reduced the intracellular lipid content in HepG2 cell line. However, this induction of MTP and ApoB by HGF was clearly inhibited by PD98059 (MAPK inhibitor). In conclusion, the data presented in this study indicated that HGF ameliorates a high-fat diet-induced fatty liver via the activation of MTP and ApoB.

Perinatal maternal high-fat diet promotes alterations in hepatic lipid metabolism and resistance to the hypolipidemic effect of fish oil in adolescent rat offspring

2016 ◽  
Vol 60 (11) ◽  
pp. 2493-2504 ◽  
Author(s):  
Lorraine S. Oliveira ◽  
Luana L. Souza ◽  
Aline F. P. Souza ◽  
Aline Cordeiro ◽  
George E. G. Kluck ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Fish Oil ◽  
High Fat Diet ◽  
Hypolipidemic Effect ◽  
High Fat ◽  
Hepatic Lipid Metabolism ◽  
Hepatic Lipid ◽  
Rat Offspring

Lactobacillus plantarum DR7 improved brain health in aging rats via the serotonin, inflammatory and apoptosis pathways

2020 ◽  
Vol 11 (8) ◽  
pp. 753-766
Author(s):  
A.I. Zaydi ◽  
L.-C. Lew ◽  
Y.-Y. Hor ◽  
M.H. Jaafar ◽  
L.-O. Chuah ◽  
...  
Keyword(s):  
Lactobacillus Plantarum ◽  
Cognitive Functions ◽  
High Fat Diet ◽  
Normal Diet ◽  
Sprague Dawley ◽  
Brain Health ◽  
High Fat ◽  
Dietary Strategy ◽  
Apoptosis Pathways ◽  
Insight Into

Aging processes affect the brain in many ways, ranging from cellular to functional levels which lead to cognitive decline and increased oxidative stress. The aim of this study was to investigate the potentials of Lactobacillus plantarum DR7 on brain health including cognitive and memory functions during aging and the impacts of high fat diet during a 12-week period. Male Sprague-Dawley rats were separated into six groups: (1) young animals on normal diet (ND, (2) young animals on a high fat diet (HFD), (3) aged animals on ND, (4) aged animals on HFD, (5) aged animals on HFD and L. plantarum DR7 (109 cfu/day) and (6) aged animals receiving HFD and lovastatin. To induce ageing, all rats in group 3 to 6 were injected sub-cutaneously at 600 mg/kg/day of D-galactose daily. The administration of DR7 has reduced anxiety accompanied by enhanced memory during behavioural assessments in aged-HFD rats (P<0.05). Hippocampal concentration of all three pro-inflammatory cytokines were increased during aging but reduced upon administration of both statin and DR7. Expressions of hippocampal neurotransmitters and apoptosis genes showed reduced expressions of indoleamine dioxygenase and P53 accompanied by increased expression of TPH1 in aged- HFD rats administered with DR7, indicating potential effects of DR7 along the pathways of serotonin and oxidative senescence. This study provided an insight into potentials of L. plantarum DR7 as a prospective dietary strategy to improve cognitive functions during aging. This study provided an insight into potentials of L. plantarum DR7 as a prospective dietary strategy to improve cognitive functions during aging.

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