The Biology of Starvation: Renal Gluconeogenesis

The Biology of Starvation

As mentioned previously, as starvation progresses the nitrogen excreted in your urine goes from predominantly urea (coming from proteolysis in early starvation) to predominantly ammonium salts (as a buffer, in late starvation). This has to happen because death by proteolysis would happen pretty soon. Proteins aren’t just skeletal muscle - they’re what make all of your organs work.

There are a lot of moving parts, here. I’m looking at you, renal gluconeogenesis.

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The ketones produced during starvation spare glucose which spares muscle. The drop in urinary urea reflects this. But ketones also show up in urine. They’re responsible for the acidosis seen in type 1 diabetes. They’re acidic and need to be buffered.

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The kidneys take up glutamine and gets two ammonia groups and a bicarbonate which can all help buffer the ketones. This process is linked with renal gluconeogenesis which produces actual glucose for the periphery, and this takes some of the gluconeogenic workload off of the liver. The increasing use of ketones also reduces hepatic gluconeogenesis.

Liver works hard in early starvation dealing with nitrogen, in later starvation it’s partially oxidizing fatty acids to produce ketones.

So, like I said above, a lot of moving parts. A lot of things need to happen simultaneously to survive starvation, and over time, we’ve gotten pretty good at it.

THIS DOES NOT MEAN INTERMITTENT FASTING IS GOOD FOR YOU

On another note, I’m in favor of three square meals a day for protein reasons. It’s easy to hit your protein goals with three meals. If you only eat 1 (not recommended) or 2 meals a day, your protein requirements actually increase, so you need to eat even more, making this either 1 binge-like feeding window or 2 huge meals. Dividing it into 3 meals is very efficient with no big further improvements beyond that.

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