AMP‐activated protein kinase signaling regulated expression of urea cycle enzymes in response to changes in dietary protein intake Article Swipe
Sandra Kirsch Heibel
,
Peter J. McGuire
,
Nantaporn Haskins
,
Himani D. Majumdar
,
Sree Rayavarapu
,
Kanneboyina Nagaraju
,
Yetrib Hathout
,
Kristy J. Brown
,
Mendel Tuchman
,
Ljubica Caldovic
·
YOU?
·
· 2019
· Open Access
·
· DOI: https://doi.org/10.1002/jimd.12133
YOU?
·
· 2019
· Open Access
·
· DOI: https://doi.org/10.1002/jimd.12133
Abundance of urea cycle enzymes in the liver is regulated by dietary protein intake. Although urea cycle enzyme levels rise in response to a high‐protein (HP) diet, signaling networks that sense dietary protein intake and trigger changes in expression of urea cycle genes have not been identified. The aim of this study was to identify signaling pathway(s) that respond to changes in protein intake and regulate expression of urea cycle genes in mice and human hepatocytes. Mice were adapted to either HP or low‐protein diets followed by isolation of liver protein and mRNA and integrated analysis of the proteomic and transcriptomic data. HP diet led to increased expression of mRNA and enzymes in amino acid degradation pathways and decreased expression of mRNA and enzymes in carbohydrate and fat metabolism, which implicated adenosine monophosphate‐activated protein kinase (AMPK) as a possible regulator. Primary human hepatocytes, treated with 5‐aminoimidazole‐4‐carboxamide ribonucleotide (AICAR) an activator of AMPK, were used to test whether AMPK regulates expression of urea cycle genes. The abundance of carbamoylphosphate synthetase 1 and ornithine transcarbamylase mRNA increased in hepatocytes treated with AICAR, which supports a role for AMPK signaling in regulation of the urea cycle. Because AMPK is either a target of drugs used to treat type‐2 diabetes, these drugs might increase the expression of urea cycle enzymes in patients with partial urea cycle disorders, which could be the basis of a new therapeutic approach.
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Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1002/jimd.12133
- OA Status
- green
- Cited By
- 11
- References
- 54
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W2951328796
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W2951328796Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1002/jimd.12133Digital Object Identifier
- Title
-
AMP‐activated protein kinase signaling regulated expression of urea cycle enzymes in response to changes in dietary protein intakeWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2019Year of publication
- Publication date
-
2019-06-09Full publication date if available
- Authors
-
Sandra Kirsch Heibel, Peter J. McGuire, Nantaporn Haskins, Himani D. Majumdar, Sree Rayavarapu, Kanneboyina Nagaraju, Yetrib Hathout, Kristy J. Brown, Mendel Tuchman, Ljubica CaldovicList of authors in order
- Landing page
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https://doi.org/10.1002/jimd.12133Publisher landing page
- Open access
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YesWhether a free full text is available
- OA status
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greenOpen access status per OpenAlex
- OA URL
-
https://www.ncbi.nlm.nih.gov/pmc/articles/7385982Direct OA link when available
- Concepts
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Enzyme, Urea cycle, Signal transduction, Protein kinase A, Urea, Protein expression, Internal medicine, Biochemistry, Endocrinology, Chemistry, Biology, Medicine, Gene, Amino acid, ArginineTop concepts (fields/topics) attached by OpenAlex
- Cited by
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11Total citation count in OpenAlex
- Citations by year (recent)
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2025: 2, 2024: 1, 2023: 1, 2022: 4, 2021: 1Per-year citation counts (last 5 years)
- References (count)
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54Number of works referenced by this work
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.(AICAR) | 148 |
| abstract_inverted_index.Because | 194 |
| abstract_inverted_index.Primary | 141 |
| abstract_inverted_index.adapted | 79 |
| abstract_inverted_index.changes | 37, 61 |
| abstract_inverted_index.dietary | 12, 32 |
| abstract_inverted_index.enzymes | 5, 112, 124, 216 |
| abstract_inverted_index.intake. | 14 |
| abstract_inverted_index.partial | 220 |
| abstract_inverted_index.protein | 13, 33, 63, 91, 134 |
| abstract_inverted_index.respond | 59 |
| abstract_inverted_index.treated | 144, 178 |
| abstract_inverted_index.trigger | 36 |
| abstract_inverted_index.whether | 157 |
| abstract_inverted_index.Abstract | 0 |
| abstract_inverted_index.Although | 15 |
| abstract_inverted_index.analysis | 96 |
| abstract_inverted_index.followed | 86 |
| abstract_inverted_index.identify | 55 |
| abstract_inverted_index.increase | 210 |
| abstract_inverted_index.networks | 29 |
| abstract_inverted_index.pathways | 117 |
| abstract_inverted_index.patients | 218 |
| abstract_inverted_index.possible | 139 |
| abstract_inverted_index.regulate | 66 |
| abstract_inverted_index.response | 22 |
| abstract_inverted_index.supports | 182 |
| abstract_inverted_index.type‐2 | 205 |
| abstract_inverted_index.Abundance | 1 |
| abstract_inverted_index.abundance | 166 |
| abstract_inverted_index.activator | 150 |
| abstract_inverted_index.adenosine | 132 |
| abstract_inverted_index.approach. | 233 |
| abstract_inverted_index.decreased | 119 |
| abstract_inverted_index.diabetes, | 206 |
| abstract_inverted_index.increased | 107, 175 |
| abstract_inverted_index.isolation | 88 |
| abstract_inverted_index.ornithine | 172 |
| abstract_inverted_index.proteomic | 99 |
| abstract_inverted_index.regulated | 10 |
| abstract_inverted_index.regulates | 159 |
| abstract_inverted_index.signaling | 28, 56, 187 |
| abstract_inverted_index.disorders, | 223 |
| abstract_inverted_index.expression | 39, 67, 108, 120, 160, 212 |
| abstract_inverted_index.implicated | 131 |
| abstract_inverted_index.integrated | 95 |
| abstract_inverted_index.pathway(s) | 57 |
| abstract_inverted_index.regulation | 189 |
| abstract_inverted_index.regulator. | 140 |
| abstract_inverted_index.synthetase | 169 |
| abstract_inverted_index.degradation | 116 |
| abstract_inverted_index.hepatocytes | 177 |
| abstract_inverted_index.identified. | 47 |
| abstract_inverted_index.metabolism, | 129 |
| abstract_inverted_index.therapeutic | 232 |
| abstract_inverted_index.carbohydrate | 126 |
| abstract_inverted_index.hepatocytes, | 143 |
| abstract_inverted_index.hepatocytes. | 76 |
| abstract_inverted_index.low‐protein | 84 |
| abstract_inverted_index.high‐protein | 25 |
| abstract_inverted_index.ribonucleotide | 147 |
| abstract_inverted_index.transcriptomic | 101 |
| abstract_inverted_index.transcarbamylase | 173 |
| abstract_inverted_index.carbamoylphosphate | 168 |
| abstract_inverted_index.monophosphate‐activated | 133 |
| abstract_inverted_index.5‐aminoimidazole‐4‐carboxamide | 146 |
| cited_by_percentile_year.max | 97 |
| cited_by_percentile_year.min | 89 |
| corresponding_author_ids | https://openalex.org/A5015939038 |
| countries_distinct_count | 1 |
| institutions_distinct_count | 10 |
| corresponding_institution_ids | https://openalex.org/I1336742384 |
| citation_normalized_percentile.value | 0.67626587 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |