Ketones, Re-Feeding and Starvation

Ketones, Re-Feeding and Starvation
When a person is not starving, carbs give them most of the energy they need. Carbohydrates are broken down into glucose, which is then actively moved along with salt against a concentration gradient. When it diffuses into the portal circulation, the blood sugar level goes up, which makes the hormone insulin make more. Insulin makes it easier for glucose to be taken in and stored. When glycogen can’t hold any more glucose, the remaining glucose is turned into fat through a process called lipogenesis, which only uses glucose that hasn’t been used up. This causes insulin and blood sugar levels to drop. (Gonzalez & Betts, 2019).

But after two or three days of being hungry, the glucose level drops. This makes the peptide hormone glucagon and makes insulin less likely to be released. Glucose levels are kept steady by glycogenolysis, but glycogen reserves run out in the first 72 hours. This changes the balance of glucose in the body, which is important for the necessary glucose cells to work. To meet this need, the liver goes through a process called gluconeogenesis, in which non-carbohydrate sources are turned into glucose. (Steinhauser et al., 2017). According to Puchalska and Crawford (2017), a muscle protein called Alanine is involved in this process, and the oxidation of fatty acids makes ketone bodies. The Krebs cycle turns acetyl coenzyme A into ketone bodies. This is how energy is made. The ketone bodies give the brain most of its energy and make it need much less glucose. Cori’s cycle is also used to make energy from the results of glycolysis, which are pyruvate and lactate. So, when a person is hungry, their metabolism changes in many ways to make sure they can get enough energy from fats to stay alive. But as a result, the body loses fat, protein, and elements like phosphate that it needs to stay healthy.

Friedli et al. (2017) say that when a person who has been starved is given food again (called “refeeding”), gluconeogenesis and anabolic metabolism drop quickly. Due to a rise in insulin secretion, this drop is caused by insulin. Insulin makes it easier for magnesium, phosphate, and potassium to move from the extracellular space into the intracellular space. This makes the extracellular space have less of these ions. Refeeding also turns on the metabolic pathways that depend on carbohydrates, which boosts the need for thiamine. Also, the person is affected in important ways by the lower amounts of ions.

If the person was overweight and died of hunger, the fat stores won’t be gone when they die. This is because hunger happens when all the body’s fats are used up and proteins are the only source of energy left. However, studies have shown that in obese people, proteins can be used up first, and death can happen before all the fats are gone. (Palmiere et al., 2016)

References

Friedli, N., Stanga, Z., Sobotka, L., Culkin, A., Kondrup, J., Laviano, A., Mueller, B., & Schuetz, P. (2017). Revisiting the refeeding syndrome: Results of a systematic review. Nutrition (Burbank, Los Angeles County, Calif.), 35, 151–160. https://doi.org/10.1016/j.nut.2016.05.016

Gonzalez, J. T., & Betts, J. A. (2019). Dietary sugars, exercise and hepatic carbohydrate metabolism. The Proceedings of the Nutrition Society, 78(2), 246–256. https://doi.org/10.1017/S0029665118002604

Palmiere, C., Tettamanti, C., Augsburger, M., Burkhardt, S., Sabatasso, S., Lardi, C., & Werner, D. (2016). Postmortem biochemistry in suspected starvation-induced ketoacidosis. Journal of forensic and legal medicine, 42, 51–55. https://doi.org/10.1016/j.jflm.2016.04.013

Puchalska, P., & Crawford, P. A. (2017). Multi-dimensional Roles of Ketone Bodies in Fuel Metabolism, Signaling, and Therapeutics. Cell metabolism, 25(2), 262–284. https://doi.org/10.1016/j.cmet.2016.12.022

Steinhauser, M. L., Olenchock, B. A., O’Keefe, J., Lun, M., Pierce, K. A., Lee, H., Pantano, L., Klibanski, A., Shulman, G. I., Clish, C. B., & Fazeli, P. K. (2018). The circulating metabolome of human starvation. JCI insight, 3(16), e121434. https://doi.org/10.1172/jci.insight.121434

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