MEAT SCIENCE
·
2023
·
IF 7.1
Shengming Zhao,Xiaorui Yuan,Liu Yang,Mingming Zhu,Hanjun Ma,Yanyan Zhao
In the current study, the effects of replacing different proportions of pork back fat (0, 25, 50, 75, and 100%) with high-pressure homogenization-modified quinoa protein emulsions (HMQE) on the physicochemical, water distribution, and rheological properties of low-fat frankfurters were investigated. HMQE incorporation significantly increased the moisture, ash, protein content, pH and L ⁎ values and decreased the a ⁎ and b ⁎ values and T 2 relaxation time of the low-fat frankfurters ( P < 0.05). Of note, 50% fat substitution by HMQE yielded higher WHC , textural properties, gel strength, immobilized water percentage and G′ value of the frankfurters than others. HMQE incorporation changed the protein secondary structure from α-helix to β-sheet, forming a compact and uniform gel network structure with small cavities. Moreover, 50% fat substitution by HMQE did not affect sensory characteristics and improved the fat oxidative stability during storage. Therefore, the incorporation of HQME as a partial fat substitute resulted in nutritional benefits and quality enhancements, indicating that HQME could serve as a promising fat alternative in manufacturing low-fat frankfurters with desirable attributes.
研究领域:
食品科学
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营养学
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生物化学
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DOI
PubMed
高影响因子
FOOD CHEMISTRY
·
2024
·
IF 8.5
Abdul Mueed,He Ma,Philippe Madjirebaye,Akhtar Ali,Sajjad Ali,Jingwen Yu,Jing Li,Ze-yuan Deng
This study investigated the influence of flaxseed oil cyclolinopeptides (CLs) on lipid and protein oxidation during high-fat meat digestion. Fourteen CLs were identified in flaxseed oil through UHPLC-ESI-QTOF-MS/MS, with dominant CLA, CLB, CLE, and CLM. During in vitro digestion, CLs inhibited lipid oxidation products (lipid hydroperoxide, Malondialdehyde, and 4-hydroxynonenal) and protein carbonylation. Compared to other groups, the lipid (16.28 ± 0.35) and protein (17.5 ± 0.6) oxidation was significantly inhibited, and antioxidant activity was remarkably increased when the CLs content reached 200 mg/kg. Through untargeted lipidomic analysis using Q-Exactive, it was observed that CLs mitigated the formation of oxidized triglycerides (OxTG) products and enhanced the hydrolysis of lipids to generate sphingolipid and polyunsaturated fatty-acids enriched glycerophospholipids imparting nutritional value to meat. Electron spin-resonance and fluorescence quenching showed that primary radicals such as alkyl and alkoxy radicals during high-fat meat digestion with flaxseed oil CLs significantly mitigate their formation. These findings collectively indicate that consuming CLs enriched flaxseed oil could reduce lipid oxidation and enhance the nutritional value of high-fat meat during digestion.
研究领域:
食品科学
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营养学
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生物化学
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产品关联
DOI
PubMed
高影响因子
Acta Pharmaceutica Sinica B
·
2021
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IF 11.614
Huiling Chen,Kaiqiang Hu,Yaru Liang,Yuqi Gao,Chenye Zeng,Kang Xu,Xiaojin Shi,Liyuan Li,Yuemiao Yin,Yi Qiao,Ying Qiu,Qingfei Liu,Zhao Wang
Although primary vesical calculi is an ancient disease, the mechanism of calculi formation remains unclear. In this study, we established a novel primary vesical calculi model with d , l -choline tartrate in mice. Compared with commonly used melamine and ethylene glycol models, our model was the only approach that induced vesical calculi without causing kidney injury. Previous studies suggest that proteins in the daily diet are the main contributors to the prevention of vesical calculi, yet the effect of fat is overlooked. To assay the relationship of dietary fat with the formation of primary vesical calculi, d , l -choline tartrate-treated mice were fed a high-fat, low-fat, or normal-fat diet. Genetic changes in the mouse bladder were detected with transcriptome analysis. A high-fat diet remarkably reduced the morbidity of primary vesical calculi. Higher fatty acid levels in serum and urine were observed in the high-fat diet group, and more intact epithelia in bladder were observed in the same group compared with the normal- and low-fat diet groups, suggesting the protective effect of fatty acids on bladder epithelia to maintain its normal histological structure. Transcriptome analysis revealed that the macrophage differentiation-related gene C–X–C motif chemokine ligand 14 ( Cxcl14 ) was upregulated in the bladders of high-fat diet-fed mice compared with those of normal- or low-fat diet-fed mice, which was consistent with histological observations. The expression of CXCL14 significantly increased in the bladder in the high-fat diet group. CXCL14 enhanced the recruitment of macrophages to the crystal nucleus and induced the transformation of M2 macrophages, which led to phagocytosis of budding crystals and prevented accumulation of calculi. In human bladder epithelia (HCV-29) cells, high fatty acid supplementation significantly increased the expression of CXCL14. Dietary fat is essential for the maintenance of physiological functions of the bladder and for the prevention of primary vesical calculi, which provides new ideas for the reduction of morbidity of primary vesical calculi.
研究领域:
泌尿学
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营养学
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免疫学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
CURRENT MOLECULAR MEDICINE
·
2017
·Vol. 17
·期 5
·381-387
·
IF 2.345
Zhu F.,Guan Y.,Zhang R.
Rationale: Studies have implied the positive association of JAK2/STAT3 signaling with the onset and severity of acute pancreatitis (AP). However, definitive functional study of JAK2/STAT3 signaling in the pathogenesis of acute pancreatitis in vivo is missing and its potential as a therapeutic
target and the underlying mechanisms remain to be determined. Objectives: The aim of this study was to explore the role of JAK2/STAT3 signaling in the pathogenesis of hyperlipidemia-intensified caerulin-induced AP and its potential as a therapeutic target. Methods and Results: Using
the caerulin-induced acute pancreatitis rat model, we showed that JAK2/STAT3 signaling was activated in pancreas and systemic inflammation was increased during AP. Pharmacological suppression of JAK2 by its inhibitor AG490 robustly protected against tissue damage, attenuated JAK2/STAT3 signaling
and inflammatory responses. Local pancreatic tissue damage and phosphor- JAK2 in the pancreatic tissue were enhanced in animals fed with high fat diet compared to chow-diet fed animals. Interestingly, JAK2 inhibitor AG490 significantly inhibited pancreas necrosis and systemic inflammation
in animals fed with high fat or chow-diet, but did not affect STAT3 signaling. Conclusion: These results establish that JAK2 activation plays a significant role in the pathogenesis of caerulin-induced AP in animals on both chow and high-fat diets by regulating necrosis and systemic inflammation.
Thus, our results not only clarify novel signaling mechanisms in AP but also suggest that JAK2 might constitute a target in the management of hyperlipidemia-intensified caerulin-induced AP.
研究领域:
胃肠病学
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药理学
·
分子生物学
·
炎症
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DOI
PubMed
高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2019
·
IF 3.571
Hui Ma,Bowei Zhang,Yaozhong Hu,Jin Wang,Jingmin Liu,Renbing Qin,Shiwen Lv,Shuo Wang
Tea polyphenols (TP) possess the ability to regulate dyslipidemia and gut microbiota dysbiosis. However, the underlying mechanism is still elusive. The present study explored the intervention of TP on high fat diet induced metabolic disorders, gut microbiota dysbiosis in mice, and the underlying intestinal mechanism. As a result, TP significantly ameliorated hyperlipidemia, improved the expression levels of hepatic lipid metabolism genes, and modulated gut microbiota. The underlying mechanism was supposed to rely on the maintaining of intestinal redox state by TP. Intestinal redox related indicators were significantly correlated with the distribution of gut microbiota. An unidentified genus of Lachnospiraceae, Bacteroides, Alistipes, and Faecalibaculum were identified as the biomarkers for intestinal redox state. Importantly, different dosages of TP modulated intestinal redox state and gut microbiota in varied patterns, and an overdose intake attenuated the beneficial effects on gut health. Our findings offered novel insights into the mechanism of TP on intestinal homeostasis.
研究领域:
营养学
·
微生物学
·
药理学
·
分子生物学
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产品关联
DOI
PubMed
高影响因子
PeerJ
·
2023
·
IF 2.7
Junfeng Zhu,Gaoqi Xu,Dihong Yang,Yu Song,Yinghui Tong,Sisi Kong,Haiying Ding,Luo Fang
Background Lapatinib is an oral small-molecule tyrosine kinase inhibitor indicated for advanced or metastatic HER2-positive breast cancer. In order to reduce the treatment cost, a high-fat enteral nutrition emulsion TPF-T was selected as a dose-sparing agent for lapatinib-based therapies. This study aimed to investigate the effect of TPF-T on lapatinib pharmacokinetics. Methods First, a simple and rapid liquid chromatography tandem mass spectrometry (LC–MS/MS) method was developed to quantitatively evaluate lapatinib in rabbit plasma. The method was fully validated according to the China Pharmacopoeia 2020 guidance. Rabbits and rats were chosen as the animal models due to their low and high bile flows, respectively. The proposed LC–MS/MS method was applied to pharmacokinetic studies of lapatinib, with or without TPF-T, in rabbit and rat plasma. Results The LC–MS/MS method revealed high sensitivity and excellent efficiency. In the rabbit model, co-administration with TPF-T resulted in a 32.2% increase in lapatinib exposure. In the rat model, TPF-T had minimal influence on the lapatinib exposure. In both models, TPF-T was observed to significantly elevate lapatinib concentration in the absorption phase. Conclusion Co-administration with TPF-T had a moderate effect on increasing exposure to lapatinib. Dose sparing using a high-fat liquid diet is potentially feasible for lapatinib-based therapies.
研究领域:
药理学
·
肿瘤学
·
临床研究
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产品关联
DOI
PubMed
高影响因子
Acta Pharmaceutica Sinica B
·
2021
·
IF 11.614
Ping-Ting Xiao,Zhi-Shen Xie,Yu-Jia Kuang,Shi-Yu Liu,Chun Zeng,Ping Li,E-Hu Liu
The mammalian target of rapamycin (mTOR)-sterol regulatory element-binding proteins (SREBPs) signaling promotes lipogenesis. However, mTOR inhibitors also displayed a significant side effect of hyperlipidemia. Thus, it is essential to develop mTOR-specific inhibitors to inhibit lipogenesis. Here, we screened the endogenous inhibitors of mTOR, and identified that FKBP38 as a vital regulator of lipid metabolism. FKBP38 decreased the lipid content in vitro and in vivo via suppression of the mTOR/P70S6K/SREBPs pathway. 3,5,6,7,8,3ʹ,4ʹ-Heptamethoxyflavone (HMF), a citrus flavonoid, was found to target FKBP38 to suppress the mTOR/P70S6K/SREBPs pathway, reduce lipid level, and potently ameliorate hyperlipidemia and insulin resistance in high fat diet (HFD)-fed mice. Our findings suggest that pharmacological intervention by targeting FKBP38 to suppress mTOR/P70S6K/SREBPs pathway is a potential therapeutic strategy for hyperlipidemia, and HMF could be a leading compound for development of anti-hyperlipidemia drugs.
研究领域:
药理学
·
代谢学
·
脂质生物学
·
药物发现
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产品关联
DOI
PubMed
高影响因子
Journal of Functional Foods
·
2024
·
IF 3.8
Qiang Li,Yanbin Zheng,Jianyu Zhao,Xinyi Wei,Zongxin Shi,Haonan Fan,Chenxu Ge,Minxuan Xu,Jun Tan
Diabetic kidney disease (DKD) is a major diabetic complication and a leading cause of end-stage renal disease (ESRD), but the therapeutic strategies for DKD are still limited. Red radishes ( Raphanus sativus L.) are a rich source of natural anthocyanins that have antioxidant, anti-apoptotic and anti-inflammatory activities. In this study, we attempted to explore the effects of natural pigment anthocyanin called radish red (RR) extracted from red radishes on DKD progression and the underlying molecular mechanisms. RR dose-dependently reduced the tubular cell injury, indicated by the decreased expression of kidney injury molecule 1 (KIM1). Furthermore, releases of pro-inflammatory cytokines including interleukin-1β (IL-1β), IL-6 and tumor necrosis factor-α (TNF-α) stimulated by HF were strongly relieved by RR. Inflammatory response and pyroptosis were also identified to be induced by HF stimulation but were mitigated by RR in HK2 cells through repressing nuclear factor-κB (NF-κB) activation and NLR family, pyrin domain-containing 3 (NLRP3) inflammasome. IR and lipogenesis due to HF exposure were also significantly ameliorated by RR in HK2 cells. Mechanistically, RNA-Seq analysis showed that RR strongly depressed interleukin-1 receptor-associated kinase-1 (IRAK1)-mediated NLRP3 inflammasome, pyroptosis, IR and lipid deposition. Importantly, IRAK1 overexpression almost diminished the beneficial effects of RR, while being rescued upon NLRP3 knockdown in HF-treated HK2 cells, revealing that RR performed its nephroprotective functions in diabetic kidney via inactivating the IRAK1-NLRP3 signaling pathway. Similarly, animal studies confirmed that RR supplementation efficiently ameliorated HFF-caused metabolic disturbance, IR, renal dysfunctions in mice and improved structural kidney damage. Consistently, RR consumption dramatically reduced lipid accumulation, inflammatory response and pyroptosis in kidney tissues of HFF-challenged mice mainly through repressing IRAK1-NLRP3 axis. Our results demonstrated that dietary supplementation with RR may serve as an IRAK1-NLRP3 inhibitor for preventing and treating diabetic nephropathy.
研究领域:
药理学
·
分子生物学
·
糖尿病学
·
肾病学
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营养学
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产品关联
DOI
高影响因子
Microbiome
·
2023
·Vol. 11
·期 1
·1-20
·
IF 15.5
Sun Penghao,Wang Mengli,Liu Yong-Xin,Li Luqi,Chai Xuejun,Zheng Wei,Chen Shulin,Zhu Xiaoyan,Zhao Shanting
Background Aberrant tryptophan (Trp)-kynurenine (Kyn) metabolism has been implicated in the pathogenesis of human disease. In particular, populations with long-term western-style diets are characterized by an excess of Kyn in the plasma. Host-gut microbiota interactions are dominated by diet and are essential for maintaining host metabolic homeostasis. However, the role of western diet-disturbed gut microbiota-colonocyte interactions in Trp metabolism remains to be elucidated. Results Here, 4-week-old mice were fed with a high-fat diet (HFD), representing a typical western diet, for 4 weeks, and multi-omics approaches were adopted to determine the mechanism by which HFD disrupted gut microbiota-colonocyte interplay causing serum Trp-Kyn metabolism dysfunction. Our results showed that colonocyte-microbiota interactions dominated the peripheral Kyn pathway in HFD mice. Mechanistically, persistent HFD-impaired mitochondrial bioenergetics increased colonic epithelial oxygenation and caused metabolic reprogramming in colonites to support the expansion of Proteobacteria in the colon lumen. Phylum Proteobacteria -derived lipopolysaccharide (LPS) stimulated colonic immune responses to upregulate the indoleamine 2,3-dioxygenase 1 (IDO1)-mediated Kyn pathway, leading to Trp depletion and Kyn accumulation in the circulation, which was further confirmed by transplantation of Escherichia coli ( E.coli ) indicator strains and colonic IDO1 depletion. Butyrate supplementation promoted mitochondrial functions in colonocytes to remodel the gut microbiota in HFD mice, consequently ameliorating serum Kyn accumulation. Conclusions Our results highlighted that HFD disrupted the peripheral Kyn pathway in a gut microbiota-dependent manner and that the continuous homeostasis of gut bacteria-colonocytes interplay played a central role in the regulation of host peripheral Trp metabolism. Meanwhile, this study provided new insights into therapies against western diet-related metabolic disorders.
Video Abstract
研究领域:
营养学
·
微生物学
·
代谢学
·
免疫学
·
胃肠病学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2022
·
IF 5.895
Shu Qing Zhang,Dan Tian,Ching Yuan Hu,Yong Hong Meng
Chlorogenic acid (CGA) displays cognition-improving properties, but the underlying mechanisms remain unclear. Herein, CGA supplementation (150 mg/kg body weight) for 14 weeks significantly prevented obesity and insulin resistance, cognitive–behavioral disturbances, and synaptic dysfunction induced by a high-fat and high-fructose diet (HFFD). Moreover, CGA supplementation enhanced the expression of genes enriched in the neuroactive ligand–receptor interaction pathway and reduced inflammatory factor expressions. Furthermore, CGA treatment increased gut microbiota diversity and the level of bacterial genera producing SCFAs. CGA also decreased the concentration of energy metabolism substrates, while it increased phosphorylcholine. Finally, we observed a significant correlation among synaptic transmission genes, gut microbiota, and neurotransmission in the CGA supplementation group by targeted multiomics analysis. Together, our results supported that the alteration of gut microbiota and metabolite composition is the underlying mechanism of CGA improving cognitive function. CGA is also a promising intervention strategy to prevent HFFD-induced cognitive impairment.
研究领域:
营养神经科学
·
微生物组研究
·
代谢组学
·
神经病学
·
药理学
✓ 已验证
DOI
PubMed
高影响因子
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