If you would calculate it: ~5 liters of blood = 50 deciliters 10g glucose = 10000 milligram

so the glucose level raises by 10000mg/50dl = 200mg/dl

However, it is known that ingesting 10g glucose only raises the blood glucose level by ~40mg/dl


  • $\begingroup$ @rotaredom I was talking about putting the glucose in through ingestion, that probably solves the problem. thanks! $\endgroup$ – Fraser Jan 2 at 16:45
  • $\begingroup$ This is nearly a personal medical question, since you're asking about your blood glucose level, but it does seem like your interested in the physiology here. I'd suggest depersonalizing this question, doing a little more research, and clarifying the actual physiology question here. To point you in the right direction, you might ask yourself how plasma concentration in a living organism is different from concentration in a beaker. $\endgroup$ – De Novo Jan 2 at 22:21
  • $\begingroup$ @DeNovo the 40mg/dl are actually not personal, it's an average of most diabetics. $\endgroup$ – Fraser Jan 3 at 14:09
  • $\begingroup$ The "I" statements are a problem, and the statement of personal experience. If you depersonalize, you'll be more likely to get an authoritative answer $\endgroup$ – De Novo Jan 3 at 16:18

If you get an intravenous injection containing 10 g of glucose, all glucose will enter the blood within few seconds and your blood glucose level will temporary rise by ~200 mg/dL.

If you take 10 g of glucose by mouth, the glucose will be dissolved and distributed within the stomach and small intestine and will be gradually absorbed into the blood, let's say within 30 minutes. In this time, some glucose will already move from the blood into the cells, so you will never have 10 g of additional glucose in the blood at a given time.

The actual blood glucose rise after ingestion of 10 g of glucose is not a fixed number, but a range that depends on several factors:

The gastrointestinal tract plays a major role in the regulation of postprandial glucose profiles. Gastric emptying is a highly regulated process, which normally ensures a limited and fairly constant delivery of nutrients and glucose to the proximal gut. The subsequent digestion and absorption of nutrients are associated with the release of a set of hormones that feeds back to regulate subsequent gastric emptying and regulates the release of insulin, resulting in downregulation of hepatic glucose production and deposition of glucose in insulin-sensitive tissues. These remarkable mechanisms normally keep postprandial glucose excursions low, regardless of the load of glucose ingested.** (Role of Gut in Glucose Homeostasis, Diabete Care, 2016)

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  • $\begingroup$ Not to mention there are other fluid compartments, two other sources of incoming glucose, outgoing glucose through utilization and storage, and even renal spillage at a certain level, a well as many many gluco-regulatory hormones (beyond insulin) that control these processes, in part, to maintain a narrow window of plasma glucose concentration regardless of acute differences in oral intake. $\endgroup$ – De Novo Jan 3 at 20:40
  • $\begingroup$ Even in a fully uncontrolled type 1 diabetic state, with ketoacidosis, it's not the glucose that gets you into (acute) trouble. It's the fluid shifts, the cerebral edema and hypokalemia. So even without any insulin, the plasma compartment doesn't act like a beaker. $\endgroup$ – De Novo Jan 3 at 20:49

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