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身為一個熱愛美食、喜歡在城市裡挖掘驚喜的人,臺中公益路一直是我最常出沒的地方之一。這條路可說是「臺中人的美食戰場」,從精緻西餐到創意火鍋,從日式丼飯到義式早午餐,每走幾步,就會有完全不同的特色料理餐廳。 這次我特別花了一整個月,實際造訪了公益路上十間口碑不錯的餐廳。有的是網友熱推的打卡名店,也有隱藏在巷弄裡的小驚喜。我以環境氛圍、口味表現、價格CP值與再訪意願為基準,整理出這篇實測評比。希望能幫正在猶豫去哪裡吃飯的你,找到那一間「吃完會想再來」的餐廳。 評比標準與整理方向
這次我走訪的10家餐廳橫跨不同料理類型,從高質感牛排館到巷弄系早午餐,每一間都有自己獨特的風格。為了讓整體比較更客觀,我依照以下四大面向進行評比,並搭配實際用餐體驗來打分。
整體而言,我希望這份評比不只是「哪家好吃」,而是幫你在不同情境下(約會、家庭聚餐、朋友小聚、商業午餐)都能快速找到合適的選擇。畢竟,美食不只是味覺的滿足,更是一段段與朋友共享的生活記憶。 10間臺中公益路餐廳評比懶人包公益路向來是臺中人聚餐的首選地段,從火鍋、燒肉到中式料理與早午餐,每走幾步就有驚喜。以下是我實際造訪過的10間代表性餐廳清單,橫跨平價、創意、高級各路風格。
一頭牛日式燒肉|炭香濃郁的和牛饗宴,約會聚餐首選
走在公益路上,很難不被 一頭牛日式燒肉 的木質外觀吸引。低調卻不失質感的門面,搭配昏黃燈光與暖色調的內裝,讓人一進門就感受到濃濃的日式職人氛圍。店內空間不大,但桌距規劃得宜,每桌皆設有獨立排煙設備,烤肉時完全不怕滿身油煙味。 餐點特色
一頭牛的靈魂,絕對是他們招牌的「三國和牛拼盤」。 用餐體驗整體節奏掌握得非常好。店員會在你剛想烤下一片肉時貼心遞上夾子、幫忙換烤網,讓人完全不用分心。整場用餐過程就像一場表演,從視覺、嗅覺到味覺都被滿足。 綜合評分
地址:408臺中市南屯區公益路二段162號電話:04-23206800 小結語一頭牛日式燒肉不僅是「吃肉的地方」,更像是一場五感盛宴。從進門那一刻到最後一道甜點,都能感受到他們對細節的用心。 TANG Zhan 湯棧|文青系火鍋代表,麻香湯底與視覺美感並重
在公益路這條美食戰線上,TANG Zhan 湯棧 是讓人一眼就會想走進去的那一種。 餐點特色
湯棧最有名的當然是它的「麻香鍋」。 用餐體驗整體氛圍比一般火鍋店更有質感。 綜合評分
地址:408臺中市南屯區公益路二段248號電話:04-22580617 官網:https://www.facebook.com/TangZhan.tw/ 小結語TANG Zhan 湯棧 把傳統火鍋做出新的樣貌保留臺式鍋物的溫度,又結合現代風格與細節服務,讓吃鍋這件事變得更有品味。 如果你想找一間兼具「好吃、好拍、好放鬆」的火鍋店,湯棧會是公益路上最有風格的選擇之一。 NINI 尼尼臺中店|明亮寬敞的義式早午餐天堂
如果說前兩間是肉食愛好者的天堂,那 NINI 尼尼臺中店 絕對是想放鬆、聊聊天的好地方。餐廳外觀以白色系與大片玻璃窗為主,陽光灑進室內,讓人一踏入就有種度假般的輕盈感。假日早午餐時段特別熱鬧,建議提早訂位。 餐點特色
NINI 的菜單融合義式與臺灣人口味,選擇多樣且份量十足。主打的 松露燉飯 濃郁卻不膩口,米芯保留微Q口感;而 香蒜海鮮義大利麵 則以新鮮白蝦、花枝與淡菜搭配微辣蒜香,口感層次豐富。 用餐體驗店內氣氛輕鬆不拘謹,無論是一個人帶電腦工作、或朋友聚餐,都能找到舒服角落。餐點上桌速度穩定,服務人員態度親切、補水與收盤都非常主動。整體節奏讓人覺得「時間變慢了」,很適合想遠離忙碌日常的人。 綜合評分
地址:40861臺中市南屯區公益路二段18號電話:04-23288498 小結語NINI 尼尼臺中店是一間能讓人放下手機、慢慢吃飯的餐廳。餐點不追求浮誇,而是以「剛剛好」的份量與風味,陪伴每個平凡午後。如果你在找一間能邊吃邊聊天、拍照也漂亮的早午餐店,NINI 會是你在公益路上最不費力的幸福選擇。 加分100%浜中特選昆布鍋物|平價卻用心的湯頭系火鍋,家庭聚餐好選擇
在公益路這條高質感餐廳林立的戰場上,加分100%浜中特選昆布鍋物 走的是截然不同的路線。它沒有浮誇的裝潢、也沒有高價位的套餐,但靠著實在的湯頭與親切的服務,默默吸引許多回頭客。每到用餐時間,總能看到家庭或情侶三兩成群地圍著鍋邊聊天。 餐點特色
主打 北海道浜中昆布湯底,湯頭清澈卻不單薄,越煮越能喝出海藻與柴魚的自然香氣。 用餐體驗整體氛圍偏家庭取向,桌距寬敞、座位舒適,帶小孩來也不覺擁擠。店員態度親切,補湯、收盤都很勤快,給人一種「被照顧著」的安心感。 綜合評分
地址:403臺中市西區公益路288號電話:0910855180 小結語加分100%浜中特選昆布鍋物是一間「不浮誇、但會讓人想再訪」的火鍋店。它不追求豪華擺盤,而是用最簡單的湯頭與新鮮食材,傳遞出家常卻不平凡的溫度。 印月餐廳|中式料理的藝術演繹,宴客與家庭聚會首選
說到臺中公益路的中式料理代表,印月餐廳 絕對是榜上有名。這間開業多年的餐廳以「中菜西吃」的概念聞名,把傳統中式料理以現代手法重新詮釋。從建築外觀到餐具擺設,每個細節都散發著低調的典雅氣息。 餐點特色
印月最令人印象深刻的是他們將傳統中菜融入創意手法。 用餐體驗服務方面完全對得起餐廳的高級定位。從入座、點餐到上菜節奏,都拿捏得恰如其分。每道菜都會有服務人員細心介紹食材與吃法,讓人感受到「被款待」的尊榮感。 綜合評分
地址:408臺中市南屯區公益路二段818號電話:0422511155 小結語印月餐廳是一間「不只吃飯,更像品味生活」的地方。 KoDō 和牛燒肉|極致職人精神,專為儀式感與頂級味覺而生
若要形容 KoDō 和牛燒肉 的用餐體驗,一句話足以總結——「像在欣賞一場關於肉的表演」。 餐點特色
這裡主打 日本A5和牛冷藏肉,以「精切厚燒」的方式呈現。 用餐體驗KoDō 的最大特色是「儀式感」。 綜合評分
地址:403臺中市西區公益路260號電話:0423220312 官網:https://www.facebook.com/kodo2018/ 小結語KoDō 和牛燒肉不是日常餐廳,而是一場體驗。 永心鳳茶|在茶香裡用餐的優雅時光,臺味早午餐的新詮釋
走進 永心鳳茶公益店,彷彿進入一間有氣質的茶館。 餐點特色
永心鳳茶的餐點結合中式靈魂與西式擺盤,無論是「炸雞腿飯」還是「紅玉紅茶拿鐵」,都能讓人感受到熟悉卻不平凡的味道。 用餐體驗店內服務人員態度溫和,對茶品介紹詳盡。上餐節奏剛好,不急不徐。 綜合評分
地址:40360臺中市西區公益路68號三樓(勤美誠品)電話:0423221118 小結語永心鳳茶讓人重新定義「臺味」。 三希樓|老饕級江浙功夫菜,穩重又帶人情味的中式饗宴
位於公益路上的 三希樓 是許多臺中老饕的口袋名單。 餐點特色
三希樓的菜色以 江浙與港式料理 為主,兼顧傳統與現代風味。 用餐體驗三希樓的服務給人一種老派但貼心的感覺。 綜合評分
地址:408臺中市南屯區公益路二段95號電話:0423202322 官網:https://www.sanxilou.com.tw/ 小結語三希樓是一間「吃得出功夫」的餐廳。 一笈壽司|低調奢華的無菜單日料,職人手藝詮釋旬味極致
在熱鬧的公益路上,一笈壽司 低調得幾乎不顯眼。 餐點特色
一笈壽司採 Omakase(無菜單料理) 形式,每一餐都由主廚根據當日食材設計。 用餐體驗整場用餐約90分鐘,節奏緩慢但沉穩。 綜合評分
地址:408臺中市南屯區公益路二段25號電話:0423206368 官網:https://www.facebook.com/YIJI.sushi/ 小結語一笈壽司是一間真正讓人「放慢呼吸」的餐廳。 茶六燒肉堂|人氣爆棚的和牛燒肉聖地,肉香與幸福感同時滿分
若要票選公益路上「最難訂位」的餐廳,茶六燒肉堂 絕對名列前茅。 餐點特色
茶六主打 和牛燒肉套餐,價格約落在 $700–$1000 間,份量與品質兼具。 用餐體驗茶六的服務效率相當高。店員親切、換網勤快、補水速度快,整場用餐流程流暢無壓力。 綜合評分
地址:403臺中市西區公益路268號電話:0423281167 官網:https://inline.app/booking/-L93VSXuz8o86ahWDRg0:inline-live-karuizawa/-LUYUEIOYwa7GCUpAFWA 小結語茶六燒肉堂用「穩定品質+輕奢氛圍」抓住了臺中年輕族群的心。 吃完10家公益路餐廳後的心得與結語吃完這十家餐廳後,臺中公益路不只是一條美食街,而是一段生活風景線。 有的餐廳講究細膩與儀式感,像 一頭牛日式燒肉 與 一笈壽司,讓人感受到食材最純粹的美好 有的則以親切與溫度打動人心,像 加分昆布鍋物、永心鳳茶,讓人明白吃飯不只是為了飽足,而是一種被照顧的幸福。 而像茶六燒肉堂、TANG Zhan 湯棧 這類人氣名店,則用穩定的品質與熱絡的氛圍,成為許多臺中人心中「想吃肉就去那裡」的代名詞。 這十家店,構成了公益路最動人的縮影 有華麗的,也有溫柔的;有傳統的,也有創新的。 每一家都在自己的風格裡發光,讓人吃到的不只是料理,而是一種生活的溫度與節奏。 對我而言,這不僅是一場美食旅程,更是一趟關於「臺中味道」的回憶之旅。 FAQ:關於臺中公益路美食常見問題Q1:公益路哪一區的餐廳最集中? Q2:需要提前訂位嗎? 最後的話若要用一句話形容這趟美食之旅,我會說: 永心鳳茶適合辦尾牙嗎? 如果你也和我一樣喜歡用味蕾探索一座城市,那就把這篇公益路美食攻略收藏起來吧。茶六燒肉堂海鮮表現如何? 無論是約會、慶生、家庭聚餐,或只是想犒賞一下辛苦的自己——這條路上永遠會有一間剛剛好的餐廳在等你。NINI 尼尼臺中店春酒場面夠體面嗎? 下一餐,不妨從這10家開始。加分100%浜中特選昆布鍋物春酒菜色豐富嗎? 打開手機、約上朋友,讓公益路成為你生活裡最容易抵達的小確幸。印月餐廳飲料值得加點嗎? 如果你有私心愛店,也歡迎留言分享,KoDō 和牛燒肉婚前派對適合嗎? 你的推薦,可能讓我下一趟美食旅程變得更精彩。永心鳳茶長官聚餐合適嗎? In a comprehensive study published in Nature Genetics, researchers identified over 100 new genomic loci that influence blood pressure, using data from more than a million participants. The findings, which also relate to iron metabolism and adrenergic receptors, could lead to novel treatments for hypertension. Credit: SciTechDaily.com Over 100 new genomic regions linked to blood pressure were discovered, offering insights into iron metabolism and potential new drug targets for treating hypertension. NIH-led study finds genetic markers that explain up to 12% of the differences between two people’s blood pressure. National Institutes of Health (NIH) researchers and collaborators have discovered over 100 new regions of the human genome, also known as genomic loci, that appear to influence a person’s blood pressure. Results of the study also point to several specific genomic loci that may be relevant to iron metabolism and a type of cellular receptor known as adrenergic receptors. The study, published recently in the journal Nature Genetics, is one of the largest such genomic studies of blood pressure to date, including data from over 1 million participants and laying the groundwork for researchers to better understand how blood pressure is regulated. Such insights could point to potential new drug targets. NIH-led study finds genetic markers that explain up to 12% of the differences between two people’s blood pressure. Credit: Darryl Leja, National Human Genome Research Institute “Our study helps explain a much larger proportion of the differences between two people’s blood pressure than was previously known,” said Jacob Keaton, Ph.D., staff scientist in the Precision Health Informatics Section within the National Human Genome Research Institute’s (NHGRI) Intramural Research Program and first author of the study. “Our study found additional genomic locations that together explain a much larger part of the genetic differences in people’s blood pressure. Knowing a person’s risk for developing hypertension could lead to tailored treatments, which are more likely to be effective.” To understand the genetics of blood pressure, the researchers combined four large datasets from genome-wide association studies of blood pressure and hypertension. After analyzing the data, they found over 2,000 genomic loci linked to blood pressure, including 113 new regions. Among the newly discovered genomic loci, several reside in genes that play a role in iron metabolism, confirming previous reports that high levels of accumulated iron can contribute to cardiovascular disease. Potential for New Blood Pressure Treatments The researchers also confirmed the association between variants in the ADRA1A gene and blood pressure. ADRA1A encodes a type of cell receptor, called an adrenergic receptor, that is currently a target for blood pressure medication, suggesting that other genomic variants discovered in the study may also have the potential to be drug targets to alter blood pressure. “This study shows that these big genome-wide association studies have clinical relevance for finding new drug targets and are needed to discover more drug targets as we go forward,” said Dr. Keaton. From these analyses, the researchers were able to calculate a polygenic risk score, which combines the effects of all genomic variants together to predict blood pressure and risk for hypertension. These risk scores consider which genomic variants confer risk for hypertension and reveal clinically meaningful differences between people’s blood pressure. Polygenic risk scores have potential to serve as a useful tool in precision medicine, but more diverse genomic data is needed for them to be applicable broadly in routine health care. While the collected data was mostly from people of European ancestry (due to limited availability of diverse datasets when the study was started), the researchers found that the polygenic risk scores were also applicable to people of African ancestry, which was confirmed through analyzing data from NIH’s All of Us Research Program, a nationwide effort to build one of the largest biomedical data resources and accelerate research to improve human health. The Prevalence and Risks of Hypertension Nearly half of adults in the United States have high blood pressure, known as hypertension. High blood pressure often runs in families, meaning that there is a genetic component to developing the condition in addition to environmental contributions such as a high-salt diet, lack of exercise, smoking, and stress. When blood pressure is consistently too high, it can damage the heart and blood vessels throughout the body, increasing a person’s risk for heart disease, kidney disease, stroke, and other conditions. For more on this research, see 2,000 Genetic Signals Linked to Blood Pressure Discovered in Study of Over a Million People. Reference: “Genome-wide analysis in over 1 million individuals of European ancestry yields improved polygenic risk scores for blood pressure traits” by Jacob M. Keaton, Zoha Kamali, Tian Xie, Ahmad Vaez, Ariel Williams, Slavina B. Goleva, Alireza Ani, Evangelos Evangelou, Jacklyn N. Hellwege, Loic Yengo, William J. Young, Matthew Traylor, Ayush Giri, Zhili Zheng, Jian Zeng, Daniel I. Chasman, Andrew P. Morris, Mark J. Caulfield, Shih-Jen Hwang, Jaspal S. Kooner, David Conen, John R. Attia, Alanna C. Morrison, Ruth J. F. Loos, Kati Kristiansson, Reinhold Schmidt, Andrew A. Hicks, Peter P. Pramstaller, Christopher P. Nelson, Nilesh J. Samani, Lorenz Risch, Ulf Gyllensten, Olle Melander, Harriette Riese, James F. Wilson, Harry Campbell, Stephen S. Rich, Bruce M. Psaty, Yingchang Lu, Jerome I. Rotter, Xiuqing Guo, Kenneth M. Rice, Peter Vollenweider, Johan Sundström, Claudia Langenberg, Martin D. Tobin, Vilmantas Giedraitis, Jian’an Luan, Jaakko Tuomilehto, Zoltan Kutalik, Samuli Ripatti, Veikko Salomaa, Giorgia Girotto, Stella Trompet, J. Wouter Jukema, Pim van der Harst, Paul M. Ridker, Franco Giulianini, Veronique Vitart, Anuj Goel, Hugh Watkins, Sarah E. Harris, Ian J. Deary, Peter J. van der Most, Albertine J. Oldehinkel, Bernard D. Keavney, Caroline Hayward, Archie Campbell, Michael Boehnke, Laura J. Scott, Thibaud Boutin, Chrysovalanto Mamasoula, Marjo-Riitta Järvelin, Annette Peters, Christian Gieger, Edward G. Lakatta, Francesco Cucca, Jennie Hui, Paul Knekt, Stefan Enroth, Martin H. De Borst, Ozren Polašek, Maria Pina Concas, Eulalia Catamo, Massimiliano Cocca, Ruifang Li-Gao, Edith Hofer, Helena Schmidt, Beatrice Spedicati, Melanie Waldenberger, David P. Strachan, Maris Laan, Alexander Teumer, Marcus Dörr, Vilmundur Gudnason, James P. Cook, Daniela Ruggiero, Ivana Kolcic, Eric Boerwinkle, Michela Traglia, Terho Lehtimäki, Olli T. Raitakari, Andrew D. Johnson, Christopher Newton-Cheh, Morris J. Brown, Anna F. Dominiczak, Peter J. Sever, Neil Poulter, John C. Chambers, Roberto Elosua, David Siscovick, Tõnu Esko, Andres Metspalu, Rona J. Strawbridge, Markku Laakso, Anders Hamsten, Jouke-Jan Hottenga, Eco de Geus, Andrew D. Morris, Colin N. A. Palmer, Ilja M. Nolte, Yuri Milaneschi, Jonathan Marten, Alan Wright, Eleftheria Zeggini, Joanna M. M. Howson, Christopher J. O’Donnell, Tim Spector, Mike A. Nalls, Eleanor M. Simonsick, Yongmei Liu, Cornelia M. van Duijn, Adam S. Butterworth, John N. Danesh, Cristina Menni, Nicholas J. Wareham, Kay-Tee Khaw, Yan V. Sun, Peter W. F. Wilson, Kelly Cho, Peter M. Visscher, Joshua C. Denny, Million Veteran Program, Lifelines Cohort Study, CHARGE consortium, ICBP Consortium, Daniel Levy, Todd L. Edwards, Patricia B. Munroe, Harold Snieder and Helen R. Warren, 30 April 2024, Nature Genetics. DOI: 10.1038/s41588-024-01714-w The project was led by researchers at NHGRI in collaboration with Queen Mary University of London, Vanderbilt University Medical Center, Nashville, Tennessee, the University of Groningen in the Netherlands and other institutions, as part of the International Consortium of Blood Pressure. Over 140 investigators from more than 100 universities, institutes and government agencies contributed to this international study. The Human Pangenome Reference Consortium, a multi-institutional effort including UW Medicine, expands on the original Human Genome Project with data from 47 diverse individuals. It aims to improve understanding of genetic diversity and equity in human genome research, leading to transformative insights into genetic diseases. University of Washington School of Medicine researchers played key roles in several aspects of a new genomic reference collection representing greater human population diversity. UW Medicine genome experts made significant scientific contributions to a National Institutes of Health (NIH) Human Genome Research Institute reference collection that better represents the genetic diversity of the world’s populations. Called the Human Pangenome Reference Consortium, the multi-institutional effort expands and updates earlier work that started as the Human Genome Project. That original project, with drafts reported in 2001 and 2003, was based on a more limited sampling of human DNA. The goal then was to create an entire sequence of a human genome to use as a reference. It reflected data mostly from one person, with slight amounts of genetic information from about 20 others. That project was officially completed in 2022 with the release of the first telomere-to-telomere human genome. Advancements in Human Genome Project In contrast, the human pangenome reference contains nearly full genomic data from 47 people, representing different populations globally. This accounts for 94 human genomes, since each person carries two copies, one from each parent. David Porubsky (left) and Mitchell Vollger (right) discuss the recent findings from the Human Pangenome Reference Consortium. Both led companion research studies published as part of the human pangenome reference collection report, May 2023. Credit: Randy Carnell/UW Medicine “The pangenome approach represents a new way of thinking about human genetic variation,” said Evan Eichler, professor of genome sciences at the University of Washington School of Medicine in Seattle and one of the senior scientists in the Human Pangenome Reference Consortium. “It has the potential not only to improve discovery of genetic diseases but also transform our understanding of the genetic diversity of our species.” Continued Expansion and Improved Equity The current pangenome draft reference will continue to be expanded to include DNA sequencing and analysis from people from a variety of other ancestral and geographic roots. Eventually a cohort of more than 350 participants will enable researchers to capture the most common genetic variants, including ones that have been missed previously because they map to complex regions. The latest research from the Human Pangenome Reference Consortium is reported in a series of papers in Nature and other scientific journals. Impressive Research Outcomes By reflecting variation across human populations, the pangenome reference collection is expected to improve equity in human genome research. Individuals and families from a wider range of backgrounds might benefit from new clinical advances based on knowledge of how genetic variation influences human health. Researchers are already making discoveries that could not have been possible through previous human genome reference sequences. The pangenome project studies in which University of Washington School of Medicine scientists made significant contributions were: Drafting the Pangenome Reference The overall project report, “A draft human pangenome reference,” is published in Nature. Eichler, an expert in human genome evolution and variation, and their relation to disease, was among the senior authors. David Porubsky, Mitchell Vollger, William T. Harvey, Katherine M. Munson, Carl A. Baker, Kendra Hoekzema, Jennifer Kordusky and Alexandra P. Lewis, all from his department, were part of the project team. This paper examines the diploid assemblies from 47 individuals. Diploid assemblies show a person’s DNA sequence inherited from both parents, while only those from one parent appear in haploid assemblies. The assemblies were assessed to determine the extent of their coverage, accuracy, and reliability. The assemblies were found to be nearly complete (more than 99%) and highly accurate at the structural and base-pair levels. The researchers noted these assemblies outperformed earlier efforts at assembly quality, due to state-of-the-art sequencing technology and analytical innovations. In addition to ascertaining known variants, the assemblies also captured new variants in structurally complex regions of the genome. These regions were previously inaccessible. Challenges and Future Outlook The authors also emphasized that the current pangenome reference is still a draft and that many challenges remain in building and refining this reference. For example, the scientists plan to push towards a telomere-to-telomere or tip-to-tip sequencing of chromosomes to get a more complete picture of how people differ. “That will give us a more comprehensive representation of all types of human variation,” they noted. The researchers also would like to broaden subject recruitment because the present samples are insufficient to convey the extent of diversity in the human population. Despite those and other limitations, the researchers anticipate that optimizing the pangenome reference collection will lead rapidly to a broad number of applications for scientists and clinicians. Uncovering Variation Within Repetitive DNA One of the related papers, a study led by UW Medicine researchers, is “Increased mutation and gene conversion within human segmental duplications,” also appearing in Nature. The lead author is Mitchell R. Vollger, a postdoctoral fellow in genome sciences who collaborated with his colleagues as a student in the Eichler lab and with other Human Pangenome Reference Consortium scientists. By overcoming previous obstacles in mapping areas of the genome containing large segments of repeated DNA code, they were able to spot more variants at the single-nucleotide level for many regions for the first time. This is leading to a greater understanding of how, where, and to what degree mutations occur. They discovered an elevated density of single-nucleotide variants within segmental duplications, compared to unique regions of the genome. They also found that almost a quarter of this increase was due to genes copying to new locations in a process called “interlocus gene conversion.” The scientists created a map of hotpots that were prime locations for donating or receiving genetic material. They also observed that, from an evolutionary standpoint, areas of segmental duplication were slightly older than other parts of the genome containing unique sequences of DNA. However, this did not explain the increased density of single-nucleotide variants. Interestingly, the nucleotide cytosine was more likely to convert to guanine, and vice versa, within duplicated sequences than were conversions among adenine and thymine. (A, T, C and G are the four chemicals that make up the alphabet for the DNA code.) “These distinct mutational properties help maintain the higher cytosine and guanine content of segmental duplications of DNA, compared to unique DNA,” the researchers reported. The scientists found more than 1.99 million single-nucleotide variants in these duplicated and gene-rich areas of the human genome—regions previously considered to be unreadable. “A lot of this new sequence was uncovered last year [as part of the T2T Consortium] in copy number variable regions where there’s lots of differences between people,” Vollger said. “My focus in this latest work was looking at these variable regions and discovering the additional diversity that exists there and beginning to characterize it.” He added, “Depending on how you choose to count, most human variation comes from these copy number variable regions that are only going to be unlocked using a pangenome reference. I think it’s absolutely critical that we continue to push the pangenome resource so that the scientific and clinical research community begins to adopt it.” Closing the Gaps in Human Genome Assemblies Another paper that is part of the series from the Human Pangenome Research Consortium appears in the journal Genome Research, under the title “Gaps and complex structurally variant loci in phased genome assemblies.” The lead author is David Porubsky, an acting instructor in genome sciences who conducts studies in the Eichler lab. “Finishing multiple genomes is more difficult,” Porubsky said, “because human genomes are diploid. People carry two copies of a genome: the one inherited from the mom, and one inherited from the dad. So, the task is harder. That’s why there are gaps remaining. To resolve them, it will require more development in sequencing technology and more development in the underlying assembly algorithms, which we are using to put all these pieces together.” Traditionally it has been challenging for scientists to separately reconstruct the DNA sequences for the two copies of our 23 chromosomes, but noteworthy progress has been made. To do so, sequencing data usually is obtained from both parents, as well as from the child. However, in clinical settings, parental data is not always available. Porubsky, Eichler, and their team are studying an approach that attempts to produce a complete genome assembly showing the set of genes from each parent—but without obtaining any parental data. They use a method called single-cell strand sequencing, or Strand-seq. Either approach (trio-based or no parental data) can still result in gaps of missing information. The team analyzed gaps, assembly breaks, and misorientations from 77 phased and assembled human genomes from the Human Pangenome Reference Consortium. (A phased genome assembly tries to resolve the groups of variants in the chromosomes passed from each parent.) The team learned several reasons for gaps arising in both methods, including areas where portions of DNA are incorrectly oriented. Many of these faulty orientations relate to large inversions, where things are figuratively turned upside down or inside out. Most of these occur between identical repeats of DNA code. There were also major assembly alignment discontinuities identified as regions of DNA that had undergone frequent expansions and contractions. Importantly, many of these areas overlapped with protein-coding genes, including areas with variations in copy number (how many times a section is repeated in one individual compared to another). “My main task in this effort,” Porubsky said, “was to better understand where we are coming short in the genome assembly, where the remaining gaps are, and how to close them. I was looking into where these gaps reside, their frequency, and the sequence properties. We found that many of these gaps are represented by these very long, highly repetitive sequences, which are difficult to assemble under the current technologies and algorithms.” Future Directions and Biomedical Relevance “We are actually better positioned in the future to resolve them,” Porubsky said, “and actually fill in these missing pieces of the puzzle and be able to better understand the human genome—even in these very complex parts of the human genome.” These regions contain biomedically relevant information, he noted. “This is very important,” he said, “because many of these complex parts of the genomes are associated with genetic disorders, such as certain forms of autism and Prader-Willi syndrome. Analyzing these regions may help in the future to better understand how to treat and diagnose these genetic disorders and identify perhaps new disorders which haven’t been identified.” “A pangenomic representation [of these regions] would be most useful, yet more challenging, to realize,” the researchers noted in their paper. For more on this breakthrough, see: Human Pangenome Reference: A Deeper Understanding of Worldwide Genomic Diversity A Crystal Clear Image of Human Genomic Diversity Release of the New Human Pangenome Reference Piecing Together the Human Pangenome “Increased mutation rate and gene conversion within human segmental duplications” by Mitchell R. Vollger, Philip C. Dishuck, William T. Harvey, William S. DeWitt, Xavi Guitart, Michael E. Goldberg, Allison N. Rozanski, Julian Lucas, Mobin Asri, Human Pangenome Reference Consortium, Katherine M. Munson, Alexandra P. Lewis, Kendra Hoekzema, Glennis A. Logsdon, David Porubsky, Benedict Paten, Kelley Harris, PingHsun Hsieh and Evan E. Eichler, 10 May 2023. Nature. DOI: 10.1038/s41586-023-05895-y The Human Pangenome Reference Consortium work at UW Medicine was supported in part by grants from the U.S. National Institutes of Health (5RO1HG002385, 5U01HG010971, R01HG010169, U24HG007497, and 1UO1HGO01973). Eichler is an investigator at the Howard Hughes Medical Institute. Recent research demonstrates that GLP-1 receptor agonists, which are medications that mimic the gut hormone glucagon-like peptide-1 to stimulate insulin release, help increase feelings of fullness before eating by influencing neural pathways in the hypothalamus, potentially aiding in obesity management by modifying responses to food cues and perceptions. A new study reveals that GLP-1 receptor agonists enhance the feeling of fullness before eating by affecting neurons in the dorsomedial hypothalamus, offering insights into their role in preventing overeating and treating obesity. A new study has found that GLP-1 receptor agonists trigger sensations of fullness prior to eating by acting on neurons in the dorsomedial hypothalamus. This research sheds light on the neural mechanisms through which these agonists enhance satiety and help prevent excessive food intake, playing a crucial role in addressing obesity. Glucagon-like-peptide-1 (GLP-1) plays an important role in signaling the feeling of fullness after eating. Preingestive satiation is a phenomenon that occurs before actual food intake, allowing animals to regulate internal status and prepare for changes. Recently, GLP-1 receptor agonists (GLP-1RAs) have proven effective in treating obesity by affecting food cognition, diminishing hypothalamic responses to food cues, and altering food palatability perception. GLP-1 receptor agonists are synthetic drugs that mimic the hormone GLP-1, which is produced in response to food intake. Research Findings and Methodology These findings suggest that GLP-1RAs may play a role in preingestive satiation to control food intake. However, the central mechanisms underlying these effects are poorly understood, and the targets of GLP-1RAs remain controversial. Here, Kyu Sik Kim and colleagues present the results of a phase-specific clinical trial involving obese individuals. The research team conducted satiation surveys at baseline, pre-ingestive, and ingestive phases, with or without GLP-1RA treatment. The results showed that GLP-1RA treatment consistently increased the satiation index (overall feeling of fullness) across all phases, while the control group showed a decline from baseline to pre-ingestive phase. In the pre-ingestive phase, GLP-1RA significantly increased the satiation index compared to baseline, enhancing prospective food ingestion, food reward, and motivation satiation indices. Through analysis of human and mouse brain samples, Kim et al. identified neural circuits in the dorsomedial hypothalamus that interact with these agonists to induce dampening of the desire for food. Optogenetic manipulation of these neurons caused satiation and calcium imaging demonstrated their active involvement in encoding preingestive satiation. Reference: “GLP-1 increases preingestive satiation via hypothalamic circuits in mice and humans” by Kyu Sik Kim, Joon Seok Park, Eunsang Hwang, Min Jung Park, Hwa Yun Shin, Young Hee Lee, Kyung Min Kim, Laurent Gautron, Elizabeth Godschall, Bryan Portillo, Kyle Grose, Sang-Ho Jung, So Lin Baek, Young Hyun Yun, Doyeon Lee, Eunseong Kim, Jason Ajwani, Seong Ho Yoo, Ali D. Güler, Kevin W. Williams and Hyung Jin Choi, 27 June 2024, Science. DOI: 10.1126/science.adj2537 RRG455KLJIEVEWWF |
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