Dual Essentiality of Choline & Methionine with Dr. Heather White, Wisconsin

Podcast Topic

This Real Science Exchange episode was recorded during a webinar, which was part of a series. Watch all the presentations from this series here: https://balchem.com/animal-nutrition-health/resources-categories/real-science-lecture-series/previous-lectures/page/10/

Guests:

Dr. Heather White, University of Madison-Wisconsin

Episode 125: Dual Essentiality of Choline & Methionine with Dr. Heather White, Wisconsin

Timestamps:

This Real Science Exchange episode was recorded during a webinar, which was part of a series. Watch all the presentations from this series here: https://balchem.com/animal-nutrition-…

Early in lactation, the cow is incapable of eating enough to meet her dramatically increased requirements. As the cow’s intake decreases near calving, there are fewer nutrient contributions from dry matter intake and she must alter nutrient partitioning to meet her increased needs by mobilizing fat and muscle stores. (1:18)

Triglycerides from fat stores are broken down into non-esterified fatty acids (NEFA) and glycerol. NEFA has two different fates in the postpartum cow: to the mammary gland as a precursor for milk fat synthesis, or to the liver to be oxidized for energy production. Glycerol enters the gluconeogenic pathway in the liver as a glucose precursor. (4:41)

The capacity for the liver to use NEFA for energy is limited by the capacity of the TCA cycle. When the TCA cycle is at capacity, excess NEFA can either undergo incomplete oxidation to ketones or be repackaged back into triglycerides. If the capacity for other tissues to use ketones for energy is exceeded, then blood concentrations of ketones rise and negative outcomes from subclinical and clinical ketosis can occur. If triglycerides accumulate in the liver, negative outcomes associated with fatty liver can occur. Triglycerides can be transported out of the liver via very low-density lipoprotein (VLDL) export; however, VLDL export does not keep up with triglyceride concentration during the transition period in dairy cows, largely because of a limiting amount of phosphatidylcholine. (5:51)

Dr. White describes a series of experiments in her lab using liver cells in culture to investigate the relationship between choline supplementation and VLDL export. As choline supplementation to the cell culture increased, so did VLDL export from the cells into the media. In addition, increasing choline supplementation to the cell culture also decreased cellular triglyceride content. (10:54)

Using gene expression and radiolabeled tracers over a series of experiments, Dr. White’s group found that as choline supplementation increased, so did complete oxidation of NEFA to energy. This was accompanied by decreased incomplete oxidation to ketone bodies and decreased accumulation of lipids in the liver cells. Glucose and glycogen were also increased with increasing choline supplementation to the cell culture, and a decrease in reactive oxygen species was observed. In addition, choline-supplemented cultures exhibited an increase in metabolic pathways associated with methionine regeneration and methyl donation. (15:29)

Dr. White then details the complexity of the metabolic pathways that intersect between choline and methionine. In similar experiments supplementing cell cultures with increasing amounts of methionine and choline, there were no effects of methionine on lipid export, oxidative pathways, or glucose metabolism. The main benefit of methionine was a marked increase in glutathione production. It’s important to note that no interactions between choline and methionine were observed in this series of experiments. (19:37)

There seems to be a clear biological priority for different sets of pathways for choline and methionine. Choline seems to be influencing lipid, glucose, and oxidative pathways, while methionine is primarily serving its role as an essential amino acid for cellular protein structure and generation, acting as a methyl donor, and impacting inflammation. Importantly, both the choline and methionine results observed in cell culture are paralleled in transition dairy cow studies. (24:14)

Dr. White’s lab further investigated the impact of methionine on inflammation. When cells were challenged with LPS to provoke an inflammatory response, methionine mitigated the inflammatory response. Similar results have been observed in liver tissue samples of transition cows. Methionine mitigated inflammatory markers and increased glutathione but did not influence reactive oxygen species. Conversely, choline decreased reactive oxygen species but did not change glutathione. (27:47)

Choline and methionine are both essential nutrients, there are biological priorities for them as methyl donors, and they are not mutually exchangeable. The lack of interaction between choline and methionine in vivo or in vitro supports the idea of different biological roles for these nutrients. (32:09)

Dr. White takes questions from the webinar audience. (34:53).

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