Gluconeogenesis in goat hepatocytes is affected by calcium, ammonia and other key metabolites but not primarily through cytosolic redox state
Comparative Biochemistry and Physiology Part B: Comparative Biochemistry, ISSN: 0305-0491, Vol: 88, Issue: 1, Page: 193-201
1987
- 37Citations
- 6Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations37
- Citation Indexes37
- 37
- CrossRef7
- Captures6
- Readers6
Article Description
1.1. Gluconeogenesis from propionate and lactate was studied in caprine hepatocytes.2.2. Reducing cytosol with additions of ETOH, ammonium, or lactate decreased [2-14C]propionate conversion to glucose.3.3. Calcium oxidized the cytosol and increased gluconeogenesis from propionate by 198% and from lactate by 220%.4.4. Cells isolated from lactating does and wethers differed quantitatively in propionate conversion to glucose and response to calcium.5.5. Acetoacetate decreased and 3-OH-butyrate slightly increased glucose production from propionate.6.6. Neither ketone body had any significant effect on gluconeogenesis from lactate.7.7. Results reported herein suggest gluconeogenesis from propionate is not limited by lack of cytosolic reducing equivalents.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/0305049187901003; http://dx.doi.org/10.1016/0305-0491(87)90100-3; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0023497525&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/2960481; https://linkinghub.elsevier.com/retrieve/pii/0305049187901003; http://dx.doi.org/10.1016/0305-0491%2887%2990100-3; https://dx.doi.org/10.1016/0305-0491%2887%2990100-3
Elsevier BV
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