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Ty thể xúc tác quá trình oxi hóa β của phần lớn axit béo chuỗi ngắn, chuỗi vừa và chuỗi dài được hấp thụ từ chế độ ăn uống, và con đường này cấu thành quá trình chính mà qua đó axit béo được oxi hóa để tạo ra năng lượng. Peroxisome tham gia vào quá trình rút ngắn chuỗi oxi hóa β của các axit béo chuỗi dài và chuỗi rất dài như acyl-coenzyme (CoA), diacyl-CoAs, este CoA của eicosanoid, axit béo có nhánh methyl 2, và este CoA của các chất trung gian acid mật di- và trihydroxycoprostanoic, đồng thời trong quá trình này, chúng tạo ra H\u003Cjats:sub>2\u003C\u002Fjats:sub>O\u003Cjats:sub>2\u003C\u002Fjats:sub>. Axit béo chuỗi dài và chuỗi rất dài (VLCFAs) cũng được chuyển hóa bởi hệ thống oxi hóa ω-CYP4A cytochrome P450 thành các axit dicarboxylic, mà sẽ là substrat cho quá trình oxi hóa β của peroxisome. Hệ thống oxi hóa β của peroxisome bao gồm (a) một con đường truyền thống có khả năng xúc tác acyl-CoAs chuỗi thẳng thông qua fatty acyl-CoA oxidase, protein L-bifunctional, và thiolase, và (b) một con đường không thể kích hoạt thứ hai xúc tác quá trình oxi hóa các axit béo acyl-CoA nhánh methyl 2 thông qua branched-chain acyl-CoA oxidase (pristanoyl-CoA oxidase\u002Ftrihydroxycoprostanoyl-CoA oxidase), protein D-bifunctional, và protein vận chuyển sterol (SCP)x. Các gen mã hóa con đường oxi hóa β truyền thống trong gan được điều chỉnh chuyển hóa bởi thụ thể kích hoạt bởi peroxisome proliferator α (PPARα). Bằng chứng từ chuột thiếu PPARα, fatty acyl-CoA oxidase peroxisome và một số enzym khác trong hai con đường oxi hóa β peroxisome chỉ ra tầm quan trọng thiết yếu của PPARα và fatty acyl-CoA oxidase peroxisome truyền thống trong chuyển hóa năng lượng, và trong sự phát triển của gan nhiễm mỡ, viêm gan nhiễm mỡ và ung thư gan.\u003C\u002Fjats:p>","\u003Cjats:p>▪ Abstract  β-Oxidation occurs in both mitochondria and peroxisomes. Mitochondria catalyze the β-oxidation of the bulk of short-, medium-, and long-chain fatty acids derived from diet, and this pathway constitutes the major process by which fatty acids are oxidized to generate energy. Peroxisomes are involved in the β-oxidation chain shortening of long-chain and very-long-chain fatty acyl-coenzyme (CoAs), long-chain dicarboxylyl-CoAs, the CoA esters of eicosanoids, 2-methyl-branched fatty acyl-CoAs, and the CoA esters of the bile acid intermediates di- and trihydroxycoprostanoic acids, and in the process they generate H\u003Cjats:sub>2\u003C\u002Fjats:sub>O\u003Cjats:sub>2\u003C\u002Fjats:sub>. Long-chain and very-long-chain fatty acids (VLCFAs) are also metabolized by the cytochrome P450 CYP4A ω-oxidation system to dicarboxylic acids that serve as substrates for peroxisomal β-oxidation. The peroxisomal β-oxidation system consists of (a) a classical peroxisome proliferator–inducible pathway capable of catalyzing straight-chain acyl-CoAs by fatty acyl-CoA oxidase, L-bifunctional protein, and thiolase, and (b) a second noninducible pathway catalyzing the oxidation of 2-methyl-branched fatty acyl-CoAs by branched-chain acyl-CoA oxidase (pristanoyl-CoA oxidase\u002Ftrihydroxycoprostanoyl-CoA oxidase), D-bifunctional protein, and sterol carrier protein (SCP)x. The genes encoding the classical β-oxidation pathway in liver are transcriptionally regulated by peroxisome proliferator–activated receptor α (PPARα). Evidence derived from mice deficient in PPARα, peroxisomal fatty acyl-CoA oxidase, and some of the other enzymes of the two peroxisomal β-oxidation pathways points to the critical importance of PPARα and of the classical peroxisomal fatty acyl-CoA oxidase in energy metabolism, and in the development of hepatic steatosis, steatohepatitis, and liver cancer.\u003C\u002Fjats:p>",{"EN":1098,"VI":1099},"P\u003Cscp>EROXISOMAL\u003C\u002Fscp>β-O\u003Cscp>XIDATION AND\u003C\u002Fscp>P\u003Cscp>EROXISOME\u003C\u002Fscp>P\u003Cscp>ROLIFERATOR\u003C\u002Fscp>–A\u003Cscp>CTIVATED\u003C\u002Fscp>R\u003Cscp>ECEPTOR\u003C\u002Fscp>α: An Adaptive Metabolic System","Oxi hóa β-Peroxisome và Thụ thể được kích hoạt bởi Peroxisome Proliferator α: Một Hệ thống Thích ứng Chuyển hóa",{"VOID":1101},"11375435",{"VOID":1103},"10.1146\u002Fannurev.nutr.21.1.193","2024-12-01T10:17:07.903+00:00",[115],[1107],"VI","https:\u002F\u002Fwww.annualreviews.org\u002Fdoi\u002F10.1146\u002Fannurev.nutr.21.1.193",[1110,1129],{"id":1111,"sortIndex":25,"researcher":24,"roles":1112,"affiliations":1113,"properties":1122,"displayName":1126,"givenName":24,"familyName":24},"6a6b7357-be46-49de-a428-1211c164db51",[],[1114],{"id":1115,"sortIndex":25,"affiliation":1116,"properties":24},"a14a1363-3f25-473e-a16a-f28e1d65dade",{"id":1115,"createTime":24,"updateTime":24,"relativeEntities":1117,"slug":24,"properties":1118,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1121,"statistic":24},[],{"title":1119},{"EN":1120},"Department of Pathology, Northwestern University Medical School, Chicago, Illinois 60611, USA. jkreddy@northwestern.edu",[],{"orcid":1123,"title":1125,"openalex":1127},{"VOID":1124},"https:\u002F\u002Forcid.org\u002F0000-0002-6452-4933",{"EN":1126},"Janardan K. 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Mặc dù nhiều nghiên cứu đã khảo sát các yếu tố lối sống ảnh hưởng đến hàm lượng IMTG, kết quả đạt được còn rất không nhất quán, và những nghiên cứu cố gắng làm sáng tỏ cơ chế phía sau chuyển hóa IMTG vẫn đang ở giai đoạn đầu. Chứng cứ hiện có hạn chế cho thấy rằng các enzyme chịu trách nhiệm cho sự phân hủy lipid ở cơ xương và tổng hợp IMTG đóng một vai trò quan trọng trong việc quyết định số phận của các axit béo và do đó là nồng độ của các chuyển hóa lipid và độ nhạy insulin của cơ xương. Bài đánh giá này cung cấp một tóm tắt về kiến thức hiện tại về tác động của tập luyện cấp tính và mãn tính cũng như khẩu phần năng lượng và thành phần chất dinh dưỡng đối với chuyển hóa IMTG và các tác động lên sức khỏe chuyển hóa.","\u003Cjats:p> Intramuscular triacylglycerol (IMTG) is both a dynamic fat-storage depot that can expand during periods of elevated lipid availability and a fatty acid source that can be utilized during periods of increased energy expenditure in active individuals. Although many studies have investigated the lifestyle determinants of IMTG content, the results are far from consistent, and studies attempting to unravel the mechanisms behind IMTG metabolism are in their infancy. The limited evidence available suggests that the enzymes responsible for skeletal muscle lipolysis and IMTG synthesis play an important role in determining the fate of fatty acids and therefore the concentration of lipid metabolites and insulin sensitivity of skeletal muscle. This review provides a summary of current knowledge on the effects of acute and chronic exercise as well as energy intake and macronutrient composition of the diet upon the metabolism of IMTG and the implications for metabolic health. \u003C\u002Fjats:p>",{"EN":1567,"VI":1568},"The Effect of Exercise and Nutrition on Intramuscular Fat Metabolism and Insulin Sensitivity","Tác động của Tập luyện và Dinh dưỡng lên Chuyển hóa Mỡ Intramuscular và Độ nhạy Insulin",{"VOID":1570},"20373917",{"VOID":1572},"10.1146\u002Fannurev.nutr.012809.104817","2024-12-01T23:16:21.561+00:00",[115],[1107],"https:\u002F\u002Fwww.annualreviews.org\u002Fdoi\u002F10.1146\u002Fannurev.nutr.012809.104817",[1578,1597,1614],{"id":1579,"sortIndex":25,"researcher":24,"roles":1580,"affiliations":1581,"properties":1590,"displayName":1594,"givenName":24,"familyName":24},"4436df5a-ebfc-4e1f-bfcf-94bac54d75fe",[],[1582],{"id":1583,"sortIndex":25,"affiliation":1584,"properties":24},"1bd8ea71-b121-4ab5-a716-ce3216a481a7",{"id":1583,"createTime":24,"updateTime":24,"relativeEntities":1585,"slug":24,"properties":1586,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1589,"statistic":24},[],{"title":1587},{"EN":1588},"School of Sport and Exercise Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT United Kingdom. c.s.shaw@bham.ac.uk",[],{"orcid":1591,"title":1593,"openalex":1595},{"VOID":1592},"https:\u002F\u002Forcid.org\u002F0000-0003-1499-0220",{"EN":1594},"Christopher S. 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neuroscience, neurodegenerative diseases, Parkinson's disease, Huntington's disease",{"VOID":2133},"6525788",{"VOID":2135},"W2117821054",{"VI":2137,"EN":2138},"\u003Cjats:p> Việc hiểu biết về sinh học mangan (Mn), đặc biệt là cơ chế điều hòa tế bào của nó và vai trò trong các bệnh thần kinh, đang trở thành lĩnh vực quan tâm ngày càng tăng. Mn là một vi chất dinh dưỡng thiết yếu cần thiết cho hoạt động của một tập hợp đa dạng các protein enzym (ví dụ, arginase và glutamine synthase). Mặc dù cần thiết cho sự sống, Mn sẽ trở nên độc hại nếu dư thừa. Do đó, việc duy trì mức độ Mn nội bào thích hợp là rất quan trọng. Khác với các kim loại thiết yếu khác, các cơ chế cân bằng nội mô ở cấp tế bào của Mn vẫn chưa được xác định. Trong đánh giá này, chúng tôi thảo luận về các hình thức tiếp xúc với Mn phổ biến, sự hấp thụ, và vận chuyển thông qua sự tiếp nhận\u002Ftổn thất được điều chỉnh tại ruột và hàng rào máu-não cũng như thông qua bài tiết qua mật. Chúng tôi trình bày những hiểu biết hiện tại về việc tiếp nhận và thoát của Mn trong tế bào cũng như việc lưu trữ và vận chuyển Mn ở mức độ tế bào con. Ngoài ra, chúng tôi cũng làm nổi bật các con đường phụ thuộc và phản ứng với Mn liên quan đến những bằng chứng đang gia tăng về vai trò của nó trong bệnh Parkinson và bệnh Huntington. Chúng tôi kết luận với những gợi ý cho các hướng nghiên cứu liên quan đến sức khỏe Mn trong tương lai. \u003C\u002Fjats:p>","\u003Cjats:p> The understanding of manganese (Mn) biology, in particular its cellular regulation and role in neurological disease, is an area of expanding interest. Mn is an essential micronutrient that is required for the activity of a diverse set of enzymatic proteins (e.g., arginase and glutamine synthase). Although necessary for life, Mn is toxic in excess. Thus, maintaining appropriate levels of intracellular Mn is critical. Unlike other essential metals, cell-level homeostatic mechanisms of Mn have not been identified. In this review, we discuss common forms of Mn exposure, absorption, and transport via regulated uptake\u002Fexchange at the gut and blood-brain barrier and via biliary excretion. We present the current understanding of cellular uptake and efflux as well as subcellular storage and transport of Mn. In addition, we highlight the Mn-dependent and Mn-responsive pathways implicated in the growing evidence of its role in Parkinson's disease and Huntington's disease. We conclude with suggestions for future focuses of Mn health-related research. \u003C\u002Fjats:p>",{"EN":2140,"VI":2141},"Manganese Is Essential for Neuronal Health","Manganese Là Chất Thiết Yếu Cho Sức Khỏe Thần Kinh",{"VOID":2143},"25974698",{"VOID":2145},"10.1146\u002Fannurev-nutr-071714-034419",[115],[1107],"https:\u002F\u002Fwww.annualreviews.org\u002Fdoi\u002F10.1146\u002Fannurev-nutr-071714-034419",[2150,2169,2196,2213,2230],{"id":2151,"sortIndex":25,"researcher":24,"roles":2152,"affiliations":2153,"properties":2162,"displayName":2166,"givenName":24,"familyName":24},"e1771acb-c0e5-4daa-b70c-5a35ca44a7e6",[],[2154],{"id":2155,"sortIndex":25,"affiliation":2156,"properties":24},"e29d342a-e005-4b2c-8d08-ccbe9d4bf88b",{"id":2155,"createTime":24,"updateTime":24,"relativeEntities":2157,"slug":24,"properties":2158,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2161,"statistic":24},[],{"title":2159},{"EN":2160},"Department of Neurology, Vanderbilt University, Nashville, Tennessee 37232; email: , ,",[],{"orcid":2163,"title":2165,"openalex":2167},{"VOID":2164},"https:\u002F\u002Forcid.org\u002F0000-0001-7365-357X",{"EN":2166},"Kyle J. 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Các hồng cầu mới này thay thế cho những hồng cầu cũ nhất (thông thường khoảng một phần trăm) bị thực bào và tiêu diệt mỗi ngày. Axit folic, vitamin B\u003Cjats:sub>12\u003C\u002Fjats:sub> và sắt có vai trò quan trọng trong quá trình hồi phục hồng cầu. Các nguyên bào hồng cầu cần axit folic và vitamin B\u003Cjats:sub>12\u003C\u002Fjats:sub> để tăng sinh trong quá trình phân hóa của chúng. Sự thiếu hụt axit folic hoặc vitamin B\u003Cjats:sub>12\u003C\u002Fjats:sub> sẽ ức chế quá trình tổng hợp purine và thymidylate, làm suy yếu tổng hợp ADN và dẫn đến apoptosis của nguyên bào hồng cầu, gây ra tình trạng thiếu máu do hồi phục hồng cầu không hiệu quả. Các nguyên bào hồng cầu cần một lượng lớn sắt cho quá trình tổng hợp hemoglobin. Một lượng lớn sắt được tái chế hàng ngày thông qua việc phân hủy hemoglobin từ các hồng cầu cũ đã bị tiêu diệt. Nhiều protein gần đây được xác định có liên quan đến sự hấp thụ, lưu trữ và xuất khẩu sắt không heme cũng như việc hấp thụ và sử dụng sắt của nguyên bào hồng cầu. Mức độ heme trong nguyên bào hồng cầu điều chỉnh sự hấp thụ sắt và tổng hợp globin, do đó sự thiếu hụt sắt sẽ gây ra tình trạng thiếu máu do tốc độ sản xuất bị chậm lại với các hồng cầu nhỏ hơn và ít được hemoglobin hóa hơn. \u003C\u002Fjats:p>","\u003Cjats:p> ▪ Abstract  Erythropoiesis is the process in which new erythrocytes are produced. These new erythrocytes replace the oldest erythrocytes (normally about one percent) that are phagocytosed and destroyed each day. Folate, vitamin B\u003Cjats:sub>12\u003C\u002Fjats:sub>, and iron have crucial roles in erythropoiesis. Erythroblasts require folate and vitamin B\u003Cjats:sub>12\u003C\u002Fjats:sub> for proliferation during their differentiation. Deficiency of folate or vitamin B\u003Cjats:sub>12\u003C\u002Fjats:sub> inhibits purine and thymidylate syntheses, impairs DNA synthesis, and causes erythroblast apoptosis, resulting in anemia from ineffective erythropoiesis. Erythroblasts require large amounts of iron for hemoglobin synthesis. Large amounts of iron are recycled daily with hemoglobin breakdown from destroyed old erythrocytes. Many recently identified proteins are involved in absorption, storage, and cellular export of nonheme iron and in erythroblast uptake and utilization of iron. Erythroblast heme levels regulate uptake of iron and globin synthesis such that iron deficiency causes anemia by retarded production rates with smaller, less hemoglobinized erythrocytes. \u003C\u002Fjats:p>",{"EN":3268,"VI":3269},"NEW INSIGHTS INTO ERYTHROPOIESIS: The Roles of Folate, Vitamin B\u003Csub>12\u003C\u002Fsub>, and Iron","CÁC KIẾN THỨC MỚI VỀ QUÁ TRÌNH HỒI PHỤC HỒNG CẦU: Vai Trò Của Axit Folic, Vitamin B\u003Csub>12\u003C\u002Fsub> Và Sắt",{"VOID":3271},"15189115",{"VOID":3273},"10.1146\u002Fannurev.nutr.24.012003.132306","2024-12-11T10:06:58.547+00:00",[115],[1107],"https:\u002F\u002Fwww.annualreviews.org\u002Fdoi\u002F10.1146\u002Fannurev.nutr.24.012003.132306",[3279,3298],{"id":3280,"sortIndex":25,"researcher":24,"roles":3281,"affiliations":3282,"properties":3291,"displayName":3295,"givenName":24,"familyName":24},"66824b46-ab0a-4420-b2d7-a302b4301bf9",[],[3283],{"id":3284,"sortIndex":25,"affiliation":3285,"properties":24},"53e994ad-0241-4e2b-87f7-90f1b098a575",{"id":3284,"createTime":24,"updateTime":24,"relativeEntities":3286,"slug":24,"properties":3287,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":3290,"statistic":24},[],{"title":3288},{"EN":3289},"Department of Medicine, Vanderbilt University School of Medicine and Veterans Affairs Tennessee Valley Healthcare System, Nashville, Tennessee 37232, USA.",[],{"orcid":3292,"title":3294,"openalex":3296},{"VOID":3293},"https:\u002F\u002Forcid.org\u002F0000-0002-7303-7694",{"EN":3295},"Mark J. 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Chem., 262, 8235, 10.1016\u002FS0021-9258(18)47554-0",{"doi":3744},"10.1016\u002FS0021-9258(18)47554-0",{"id":24,"text":3746,"url":24,"identifiers":3747},"10.1074\u002Fjbc.C000905200",{"doi":3746},{"id":24,"text":3749,"url":24,"identifiers":3750},"10.1073\u002Fpnas.59.2.582",{"doi":3749},{"id":3752,"createTime":3753,"updateTime":3754,"relativeEntities":3755,"slug":3756,"properties":3757,"entityType":111,"verifyStatus":112,"verifyTime":3772,"verifyNote":113,"languages":3773,"translateLanguages":3774,"viewCount":25,"primaryUrl":3775,"fullTextUrl":24,"authors":3776,"publicationType":157,"publisherRelationship":3811,"citationCount":3860,"citationInfo":3861,"publishDate":3868,"publishYear":3862,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":3869,"openAccess":24,"references":3870,"isForceReanalyzing":224},"2b073b4b-a661-45c5-9a30-cdd27453a305","2024-12-11T10:09:33.654+00:00","2025-01-09T20:29:52.443+00:00",[],"C-scp-ERULOPLASMIN-scp-M-scp-ETABOLISM-AND-scp-F-scp-UNCTION-scp-",{"mag":3758,"keywords":3760,"openalex":3761,"abstract":3763,"title":3766,"pm":3769,"doi":3771},{"VOID":3759},"2146890885",{"VI":1091},{"VOID":3762},"W2146890885",{"VI":3764,"EN":3765},"\u003Cjats:p> ▪ Tóm tắt  Ceruloplasmin là một ferroxidase huyết thanh chứa hơn 95% đồng có trong huyết tương. Protein này là một thành viên của họ oxydase đa đồng, một nhóm protein được bảo toàn trong quá trình tiến hóa, sử dụng đồng để kết hợp quá trình oxi hóa cơ chất với việc khử oxy thành nước bằng bốn electron. Mặc dù cần có đồng để ceruloplasmin hoạt động, nhưng protein này không đóng vai trò thiết yếu trong việc vận chuyển hoặc chuyển hóa kim loại này. Aceruloplasminemia là một bệnh thoái hóa thần kinh do sự mất chức năng di truyền của gen ceruloplasmin. Đặc điểm của rối loạn này đã chỉ ra vai trò sinh lý quan trọng của ceruloplasmin trong việc xác định tốc độ thoát sắt từ các tế bào có kho dự trữ sắt có thể mobilizable và đã cung cấp những hiểu biết mới về chuyển hóa và dinh dưỡng sắt ở người.","\u003Cjats:p> ▪ Abstract  Ceruloplasmin is a serum ferroxidase that contains greater than 95% of the copper found in plasma. This protein is a member of the multicopper oxidase family, an evolutionarily conserved group of proteins that utilize copper to couple substrate oxidation with the four-electron reduction of oxygen to water. Despite the need for copper in ceruloplasmin function, this protein plays no essential role in the transport or metabolism of this metal. Aceruloplasminemia is a neurodegenerative disease resulting from inherited loss-of-function mutations in the ceruloplasmin gene. Characterization of this disorder revealed a critical physiological role for ceruloplasmin in determining the rate of iron efflux from cells with mobilizable iron stores and has provided new insights into human iron metabolism and nutrition. \u003C\u002Fjats:p>",{"EN":3767,"VI":3768},"C\u003Cscp>ERULOPLASMIN\u003C\u002Fscp> M\u003Cscp>ETABOLISM AND\u003C\u002Fscp> F\u003Cscp>UNCTION\u003C\u002Fscp>","Chuyển hóa và Chức năng của Ceruloplasmin",{"VOID":3770},"12055353",{"VOID":3511},"2024-12-11T10:09:33.653+00:00",[115],[1107],"https:\u002F\u002Fwww.annualreviews.org\u002Fdoi\u002F10.1146\u002Fannurev.nutr.22.012502.114457",[3777,3794],{"id":3778,"sortIndex":25,"researcher":24,"roles":3779,"affiliations":3780,"properties":3789,"displayName":3791,"givenName":24,"familyName":24},"09f412bf-9306-4232-af0e-048b799be8ab",[],[3781],{"id":3782,"sortIndex":25,"affiliation":3783,"properties":24},"ee0f54df-79a2-45b4-b6a7-cd602715069e",{"id":3782,"createTime":24,"updateTime":24,"relativeEntities":3784,"slug":24,"properties":3785,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":3788,"statistic":24},[],{"title":3786},{"EN":3787},"Edward Mallinckrodt Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri 63110, USA.",[],{"title":3790,"openalex":3792},{"EN":3791},"Nathan E. 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Chem., 266, 5128, 10.1016\u002FS0021-9258(19)67764-1",{"doi":4137},"10.1016\u002FS0021-9258(19)67764-1",{"id":24,"text":4139,"url":24,"identifiers":4140},"Schaefer M, 1999, Am. J. Physiol., 276, G311",{},{"id":24,"text":4142,"url":24,"identifiers":4143},"10.1152\u002Fajpgi.1999.276.3.G639",{"doi":4142},{"id":24,"text":4145,"url":24,"identifiers":4146},"10.1126\u002Fscience.116.3018.484",{"doi":4145},{"id":24,"text":4148,"url":24,"identifiers":4149},"10.1007\u002Fs004380050600",{"doi":4148},{"id":24,"text":4151,"url":24,"identifiers":4152},"10.1126\u002Fscience.271.5255.1552",{"doi":4151},{"id":24,"text":4154,"url":24,"identifiers":4155},"10.1172\u002FJCI104407",{"doi":4154},{"id":24,"text":4157,"url":24,"identifiers":4158},"10.1073\u002Fpnas.81.2.390",{"doi":4157},{"id":24,"text":4160,"url":24,"identifiers":4161},"Takahashi Y, 1995, Hum. Mol. Genet., 51, 81",{},{"id":24,"text":4163,"url":24,"identifiers":4164},"10.1016\u002F0925-4439(94)00072-X",{"doi":4163},{"id":24,"text":4166,"url":24,"identifiers":4167},"10.1016\u002FS0361-9230(01)00510-X",{"doi":4166},{"id":24,"text":4169,"url":24,"identifiers":4170},"10.1074\u002Fjbc.274.53.38061",{"doi":4169},{"id":24,"text":3712,"url":24,"identifiers":4172},{"doi":3712},{"id":24,"text":4174,"url":24,"identifiers":4175},"10.1165\u002Fajrcmb.14.2.8630266",{"doi":4174},{"id":24,"text":4177,"url":24,"identifiers":4178},"10.1073\u002Fpnas.83.10.3257",{"doi":4177},{"id":24,"text":4180,"url":24,"identifiers":4181},"Yang FM, 1990, J. Biol. Chem.",{},{"id":24,"text":4183,"url":24,"identifiers":4184},"10.1016\u002FS0022-510X(98)00015-X",{"doi":4183},{"id":24,"text":4186,"url":24,"identifiers":4187},"10.1159\u002F000008091",{"doi":4186},{"id":24,"text":4189,"url":24,"identifiers":4190},"10.1038\u002Fng0395-267",{"doi":4189},{"id":24,"text":4192,"url":24,"identifiers":4193},"10.1016\u002FS0022-510X(00)00295-1",{"doi":4192},{"id":24,"text":4195,"url":24,"identifiers":4196},"10.1007\u002Fs007750050018",{"doi":4195},{"id":4198,"createTime":4199,"updateTime":4200,"relativeEntities":4201,"slug":4202,"properties":4203,"entityType":111,"verifyStatus":112,"verifyTime":4219,"verifyNote":113,"languages":4220,"translateLanguages":4221,"viewCount":25,"primaryUrl":4222,"fullTextUrl":24,"authors":4223,"publicationType":157,"publisherRelationship":4260,"citationCount":4309,"citationInfo":4310,"publishDate":4315,"publishYear":4311,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":4316,"openAccess":24,"references":4317,"isForceReanalyzing":224},"8ab6e787-6e32-45ed-a863-8cc51f2fa54e","2024-12-13T20:59:06.641+00:00","2025-01-09T20:28:56.860+00:00",[],"Regulation-of-Glutaminase-Activity-and-Glutamine-Metabolism",{"mag":4204,"keywords":4206,"openalex":4207,"abstract":4209,"title":4212,"pm":4215,"doi":4217},{"VOID":4205},"2177855681",{"VI":1091},{"VOID":4208},"W2177855681",{"VI":4210,"EN":4211},"\u003Cjats:p> Glutamine được tổng hợp chủ yếu trong cơ bắp, phổi và mô mỡ. Glutamin huyết tương đóng vai trò quan trọng như một chất vận chuyển nitơ, cacbon và năng lượng giữa các cơ quan và được sử dụng cho việc tổng hợp ure ở gan, cho quá trình ammoniagenesis ở thận, cho gluconeogenesis ở cả gan và thận, và như một nguồn nhiên liệu hô hấp chính cho nhiều tế bào. Quá trình phân giải glutamin được bắt đầu bởi một trong hai isoform của glutaminase ty thể. Glutaminase kiểu gan chỉ được biểu hiện trong các tế bào hepatocyte periportal của gan sau sinh, nơi nó kết hợp hiệu quả việc sản xuất ammoniac với tổng hợp ure. Glutaminase kiểu thận phong phú trong thận, não, ruột, gan thai nhi, bạch cầu lympho và các tế bào chuyển hóa, nơi ammoniac tạo ra được giải phóng mà không cần tiếp tục chuyển hóa. Hai isoenzyme này có những đặc điểm cấu trúc và động học khác nhau góp phần vào chức năng và điều chỉnh ngắn hạn của chúng. Mặc dù có một độ đồng nhất cao trong chuỗi axit amin, hai loại glutaminase là sản phẩm của các gen khác nhau nhưng có liên quan. Hai isoenzyme này cũng chịu sự điều chỉnh dài hạn. Glutaminase gan tăng lên trong các trường hợp đói, tiểu đường, và khi ăn chế độ ăn giàu protein, trong khi glutaminase kiểu thận chỉ tăng ở thận để đáp ứng với toan chuyển hóa. Các thích ứng trong glutaminase gan được trung gian bởi các thay đổi trong tốc độ phiên mã, trong khi glutaminase kiểu thận được điều chỉnh ở cấp độ sau phiên mã.","\u003Cjats:p> Glutamine is synthesized primarily in skeletal muscle, lungs, and adipose tissue. Plasma glutamine plays an important role as a carrier of nitrogen, carbon, and energy between organs and is used for hepatic urea synthesis, for renal ammoniagenesis, for gluconeogenesis in both liver and kidney, and as a major respiratory fuel for many cells. The catabolism of glutamine is initiated by either of two isoforms of the mitochondrial glutaminase. Liver-type glutaminase is expressed only in periportal hepatocytes of the postnatal liver, where it effectively couples ammonia production with urea synthesis. Kidney­type glutaminase is abundant in kidney, brain, intestine, fetal liver, lymphocytes, and transformed cells, where the resulting ammonia is released without further metabolism. The two isoenzymes have different structural and kinetic properties that contribute to their function and short-term regulation. Although there is a high degree of identity in amino acid sequences, the two glutaminases are the products of different but related genes. The two isoenzymes are also subject to long-term regulation. Hepatic glutaminase is increased during starvation, diabetes, and feeding a high-protein diet, whereas kidney-type glutaminase is increased only in kidney in response to metabolic acidosis. The adaptations in hepatic glutaminase are mediated by changes in the rate of transcription, whereas kidney-type glutaminase is regulated at a posttranscriptional level. \u003C\u002Fjats:p>",{"EN":4213,"VI":4214},"Regulation of Glutaminase Activity and Glutamine Metabolism","Quy định hoạt động của Glutaminase và chuyển hóa Glutamin",{"VOID":4216},"8527215",{"VOID":4218},"10.1146\u002Fannurev.nu.15.070195.001025","2024-12-13T20:59:06.640+00:00",[115],[1107],"https:\u002F\u002Fwww.annualreviews.org\u002Fdoi\u002F10.1146\u002Fannurev.nu.15.070195.001025",[4224,4241],{"id":4225,"sortIndex":25,"researcher":24,"roles":4226,"affiliations":4227,"properties":4236,"displayName":4238,"givenName":24,"familyName":24},"7aa6db5f-d443-4604-9c96-a672bbbd00a2",[],[4228],{"id":4229,"sortIndex":25,"affiliation":4230,"properties":24},"1d5bcde1-0c04-40a9-966f-8f56cb5cd8ec",{"id":4229,"createTime":24,"updateTime":24,"relativeEntities":4231,"slug":24,"properties":4232,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":4235,"statistic":24},[],{"title":4233},{"VI":4234},"Department of Biochemistry and Molecular Biology, Colorado State University, Fort Collins, Colorado 80523",[],{"title":4237,"openalex":4239},{"EN":4238},"Norman P. Curthoys",{"VOID":4240},"A5108538258",{"id":4242,"sortIndex":139,"researcher":24,"roles":4243,"affiliations":4244,"properties":4253,"displayName":4257,"givenName":24,"familyName":24},"6f61ce44-eb1c-4a34-8df3-ec986a5ea276",[],[4245],{"id":4246,"sortIndex":25,"affiliation":4247,"properties":24},"b42fc00e-fda1-4082-b54e-9687f5c24b54",{"id":4246,"createTime":24,"updateTime":24,"relativeEntities":4248,"slug":24,"properties":4249,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":4252,"statistic":24},[],{"title":4250},{"EN":4251},"Department of Nutritional Sciences, Rutgers University, New Brunswick, New Jersey 08903",[],{"orcid":4254,"title":4256,"openalex":4258},{"VOID":4255},"https:\u002F\u002Forcid.org\u002F0000-0002-1275-0744",{"EN":4257},"Malcolm Watford",{"VOID":4259},"A5046035837",{"url":24,"publisher":4261,"properties":4303},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":4262,"slug":10,"properties":4263,"entityType":22,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":25,"subjectFields":4268,"manageAffiliations":4277,"indexDatabases":4288,"url":90,"thumbnailPath":24,"statistic":24,"gsStatistic":24,"type":24,"analyzePriority":24},[],{"country":4264,"eissn":4265,"issn":4266,"title":4267},{"VOID":13},{"VOID":15},{"VOID":17},{"EN":19},[4269,4273],{"id":28,"createTime":24,"updateTime":24,"relativeEntities":4270,"label":4271,"description":4272,"parentId":24,"standard":24,"scholarHubFieldId":24},[],{"EN":31},{},{"id":34,"createTime":24,"updateTime":24,"relativeEntities":4274,"label":4275,"description":4276,"parentId":24,"standard":24,"scholarHubFieldId":24},[],{"EN":37},{},[4278,4283],{"id":41,"createTime":24,"updateTime":24,"relativeEntities":4279,"slug":24,"properties":4280,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":4282,"statistic":24},[],{"title":4281},{"EN":45},[],{"id":48,"createTime":24,"updateTime":24,"relativeEntities":4284,"slug":24,"properties":4285,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":4287,"statistic":24},[],{"title":4286},{"EN":52},[],[4289,4296],{"id":56,"indexDatabase":4290,"url":67,"indexYears":68,"academicFieldIds":4295,"indexDatabaseRanking":72},{"id":58,"createTime":24,"updateTime":24,"relativeEntities":4291,"label":4292,"description":4293,"key":64,"publicationTags":4294,"standard":24},[],{"EN":61,"VI":61},{"EN":61,"VI":63},[66],[70,71],{"id":74,"indexDatabase":4297,"url":87,"indexYears":24,"academicFieldIds":4302,"indexDatabaseRanking":24},{"id":76,"createTime":24,"updateTime":24,"relativeEntities":4298,"label":4299,"description":4300,"key":83,"publicationTags":4301,"standard":24},[],{"EN":79,"VI":79},{"EN":81,"VI":82},[85,86],[89],{"issue":4304,"pages":4305,"volume":4307},{"VOID":203},{"VOID":4306},"133-159",{"VOID":4308},"15",594,{"total":4309,"publishYear":4311,"statisticByYear":4312},1995,{"2012":3374,"2013":3374,"2014":1207,"2015":3371,"2016":491,"2017":494,"2018":1201,"2019":4313,"2020":494,"2021":3374,"2022":1210,"2023":3370,"2024":4314},23,16,"1995-07-01",[85,72],[],{"id":4319,"createTime":4320,"updateTime":4321,"relativeEntities":4322,"slug":4323,"properties":4324,"entityType":111,"verifyStatus":112,"verifyTime":4320,"verifyNote":113,"languages":4340,"translateLanguages":4341,"viewCount":25,"primaryUrl":4342,"fullTextUrl":24,"authors":4343,"publicationType":157,"publisherRelationship":4380,"citationCount":4428,"citationInfo":4429,"publishDate":4315,"publishYear":4311,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":4434,"openAccess":24,"references":4435,"isForceReanalyzing":224},"af6d50f9-211c-4e17-b835-7bee9f4dfeaf","2024-12-26T11:51:22.106+00:00","2025-01-09T20:27:57.426+00:00",[],"Lactoferrin-Molecular-Structure-and-Biological-Function",{"mag":4325,"keywords":4327,"openalex":4328,"abstract":4330,"title":4333,"pm":4336,"doi":4338},{"VOID":4326},"2113423265",{"VI":1091},{"VOID":4329},"W2113423265",{"VI":4331,"EN":4332},"\u003Cjats:p> Lactoferrin là một glycoprotein liên kết với sắt có khối lượng phân tử 80-kDa, có mặt trong sữa và, ít hơn, trong các dịch tiết ngoại tiết như dịch mật và nước mắt. Nó bao gồm một polypeptide chuỗi đơn với hai thùy hình cầu và tương đối kháng lại sự phân hủy bởi protease. Các cDNA hoàn chỉnh cho lactoferrin từ sữa người, bạch cầu trung tính và sữa bò đã được báo cáo, và các protein tái tổ hợp đã được sản xuất. Nhờ vào các đặc tính liên kết với sắt, lactoferrin được đề xuất là có vai trò trong việc hấp thu sắt qua niêm mạc ruột và hoạt động như một tác nhân kìm khuẩn bằng cách giữ lại sắt từ các vi khuẩn cần sắt. Sự hiện diện của nó trong bạch cầu trung tính và việc giải phóng trong quá trình viêm cho thấy rằng lactoferrin cũng liên quan đến việc tiêu diệt thực bào và phản ứng miễn dịch. Thêm vào đó, lactoferrin có thể hoạt động theo những cách không liên quan đến việc liên kết với sắt, ví dụ như một yếu tố tăng trưởng và một tác nhân diệt khuẩn. Bài đánh giá này cố gắng đánh giá các chức năng được đề xuất này và ý nghĩa sinh học của chúng một cách chi tiết hơn. \u003C\u002Fjats:p>","\u003Cjats:p> Lactoferrin is an 80-kDa, iron-binding glycoprotein present in milk and, to a lesser extent, in exocrine fluids such as bile and tears. It consists of a single-chain polypeptide with two gobular lobes and is relatively resistant to proteolysis. The complete cDNAs for lactoferrin from human milk, neutrophils, and bovine milk have been reported, and recombinant proteins have been produced. Owing to its iron-binding properties, lactoferrin has been proposed to play a role in iron uptake by the intestinal mucosa and to act as a bacteriostatic agent by withholding iron from iron-requiring bacteria. Its presence in neutrophils and its release during inflammation suggest that lactoferrin is also involved in phagocytic killing and immune responses. Additionally, lactoferrin may function in ways not related to iron-binding, e.g. as a growth factor and as a bactericidal agent. This review attempts to evaluate these proposed functions and their biological significance in more detail. \u003C\u002Fjats:p>",{"EN":4334,"VI":4335},"Lactoferrin: Molecular Structure and Biological Function","Lactoferrin: Cấu trúc phân tử và chức năng sinh học",{"VOID":4337},"8527233",{"VOID":4339},"10.1146\u002Fannurev.nu.15.070195.000521",[115],[1107],"https:\u002F\u002Fwww.annualreviews.org\u002Fdoi\u002F10.1146\u002Fannurev.nu.15.070195.000521",[4344,4363],{"id":4345,"sortIndex":25,"researcher":24,"roles":4346,"affiliations":4347,"properties":4356,"displayName":4360,"givenName":24,"familyName":24},"d6ad2cce-a8fa-49e5-9a88-2cdb33b02c47",[],[4348],{"id":4349,"sortIndex":25,"affiliation":4350,"properties":24},"5342a353-c14e-4ec8-98d9-60435253c55d",{"id":4349,"createTime":24,"updateTime":24,"relativeEntities":4351,"slug":24,"properties":4352,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":4355,"statistic":24},[],{"title":4353},{"VI":4354},"Department of Nutrition, University of California, Davis, California 95616",[],{"orcid":4357,"title":4359,"openalex":4361},{"VOID":4358},"https:\u002F\u002Forcid.org\u002F0000-0002-3459-2484",{"EN":4360},"Bo Lönnerdal",{"VOID":4362},"A5071670795",{"id":4364,"sortIndex":139,"researcher":24,"roles":4365,"affiliations":4366,"properties":4373,"displayName":4377,"givenName":24,"familyName":24},"b0dd9199-5837-4aee-92e2-94a4409c2053",[],[4367],{"id":4349,"sortIndex":25,"affiliation":4368,"properties":24},{"id":4349,"createTime":24,"updateTime":24,"relativeEntities":4369,"slug":24,"properties":4370,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":4372,"statistic":24},[],{"title":4371},{"VI":4354},[],{"orcid":4374,"title":4376,"openalex":4378},{"VOID":4375},"https:\u002F\u002Forcid.org\u002F0000-0002-8918-7005",{"EN":4377},"Smita S. 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