Role of Muscle in CO2 Production After Oral Glucose Administration in Man

Abstract

A significant increase in CO2 production, reflecting carbohydrate oxidation and/or fat synthesis, is observed in normal subjects after the ingestion of glucose. The anatomic site(s) of this CO2 production has not yet been localized, although liver and muscle are logical considerations. To assess the contribution of skeletal muscle to this process, we measured whole-body and forearm CO2 flux in normal, postabsorptive subjects after the ingestion of 100 g of glucose and calculated their total muscle CO2 production. In the basal state, muscle accounted for 19% of total CO2 production, and, after glucose administration, muscle CO2 production did not change significantly. Thus, muscle is not the principal site of the observed increase in CO2 production.

Chronic Intermittent Intravenous Insulin Therapy: A New Frontier in Diabetes Therapy

“…25 Carbon dioxide production by the heart, 26 kidney, 27 brain, 28 and gut 29 has also been measured in other mammals, and cannot account for the large increment in total CO 2 production. Thus, both indirect in vivo human studies 23 and direct in vitro experimental data support the concept that the liver is the source of the majority of the CO 2 production associated with glucose ingestion.…”

“…After glucose administration, CO 2 production (and consequently the RQ) increases (0.9-1.0), indicating that glucose has become the primary source of energy. In contrast, in the patient with diabetes mellitus on conventional insulin therapy, no such increase in RQ 21,22 or CO 2 production 23 is observed. The possible fate of ingested glucose is (a) oxidation (liver, brain, muscle), (b) conversion to fat (liver, muscle, adipose tissue), (c) storage as glycogen (liver, muscle) or transamination of intermediary metabolites to form amino acids (e.g., alanine).…”

“…Liver and muscle appear to be the most active tissues for glucose oxidation. In 1985, Meistas et al 23 showed in nondiabetic postabsorptive men that resting muscle is not the source of the increase in CO 2 production after ingestion of a 100-g glucose meal. Glucose utilization by fat is minimal (ca.…”

“…An increase in the RQ to greater than 0.90 is used as the index of therapeutic efficacy. [21][22][23] It was postulated that if hepatic activation was achieved and maintained in patients with "brittle" IDDM by this treatment, the glycohemoglobin Alc (HbAlc) blood levels and the frequency of hypoglycemic reactions should decrease.…”

The biochemistry of diabetes

“…Following glucose ingestion, splanchnic lactate uptake changes to net output and forearm oxygen uptake and lactate balance do not change (Meistas et al, 1985;Jackson et al, 1986). These findings suggest that intestine or liver metabolizes glucose to lactate, some of which is eventually stored by the liver as glycogen and fatty acid.…”