Carbohydrate Metabolism - Carbohydrate Disposal, How Does The Body Deal With Excess Carbs?

Since de novo lipogenesis (the conversion of carbs to fat) is quantitatively unimportant in humans, how does the body get rid of the excess calories from carbs?

Let’s take a closer look at carbohydrate disposal. After glycogen depletion, glycogen stores takes up 4 days to saturate (1). Extreme carbohydrate manipulations have shown rapidly auto-regulatory adjustments in carbohydrate oxidation rates (2,3) over short periods of time, and the effect persists after normalization of the diet in response to the perturbed glycogen stores (2).

With the onset of carbohydrate overfeeding (after total glycogen depletion), there was a dramatic increase in carbohydrate oxidation from 74 ± 40 g/d (day 3) to 398 ± 87 g/d (day 4) (1). Thereafter carbohydrate utilization (ie, oxidation and that used for de novo lipid synthesis) increased progressively in response to the increase in carbohydrate ingestion, attaining 1010 ± 37 g/d on the last day of overfeeding (7 days) (1). 

By the end of the second day of overfeeding, glycogen stores had increased by 500g. At this point carbohydrate oxidation and storage became insufficient to dispose of all of the ingested carbohydrate, and some had to be converted to fat, ie, de novo lipogenesis (150g lipid/d using 475 CHO/d). This is perhaps the biggest increase in DNL ever recorded, possibly due the extreme nature of the diet with only 3% of fat and with 86% of carbohydrate. It is known that DNL increases a bit more with a diet below 10% of fats coupled with a high carb intake.

After 4 d of overfeeding glycogen stores became saturated at ~770g (occurred on day 5 for one subject). When the glycogen stores are saturated, massive intakes of carbohydrate are disposed of by high carbohydrate-oxidation rates (1).

In other metabolic ward study (12 days), carbohydrate intake of 540g and 83 g/d for overfeeding and underfeeding, respectively, exerted direct auto-regulatory feedback on carbohydrate oxidation (551 and 106 g/d at day 12 for overfeeding and underfeeding, respectively) (4).

With carbohydrate overfeeding there was a large increase in carbohydrate oxidation but also in glycogen storage (339 ± 82 g/d). Carbohydrate balance was achieved after the first few days and by day 12 carbohydrate oxidation was 551 g/d compared with an intake of 539 g/d. Carbohydrate oxidation was providing ~8.68 MJ/d, thus fat oxidation was suppressed. During overfeeding, BMR increased by 0.42 MJ (5.7%) and TEE increased by 0.75 MJ (6.2%).

This study also performed underfeeding. As expected over the first few days of underfeeding there was a sharp decrease in carbohydrate oxidation, reflecting a gradual but progressive decrease in muscle glycogen. After day 4 carbohydrate intake and oxidation were closely matched, with a small, persistent daily negative carbohydrate balance with intakes of 83 g/d compared with oxidation of 106 g/d (1.67 MJ/d) on day 12. In this case, to meet the body’s energy requirement endogenous fat oxidation increased. BMR decreased by 0.82 MJ (8.3%) and TEE decreased by 1.20 MJ (10.5%).

The contribution of protein to the fuel mixture during both interventions remained remarkably constant.


Progressive carbohydrate oxidation and total energy expenditure increases are seen with carbohydrate overfeeding (50% of excess energy intake) (5). Carbohydrate oxidation and total energy expenditure increases were evident in the first day of overfeeding and reached maximum by day 7 of overfeeding (14 days total). 

The increased energy expenditure was approximately double that which could be explained by the combination of increased TEF and increased body mass, meaning that more of the excess energy was oxidized and less stored in the body than was seen during fat overfeeding (5). 

Even on day 14 total energy expenditure was higher with carbohydrate overfeeding so that the total stored energy was less than with fat overfeeding.

This study also compared lean vs. obese subjects, and it was noted that obese subjects oxidized proportionally more carbohydrate and less fat than did lean subjects (5). The greatest reliance on carbohydrate oxidation during energy balance perturbations may be a risk factor for obesity (6,7,8). Subjects with the highest oxidative capacity of skeletal muscle have the lowest ratio of fat to lean mass in weight gain (9).

Another study showed a graded dose response in carbohydrate oxidation (10). Researchers used stable isotope-mass spectrometric methods with indirect calorimetry in normal subjects to quantify the metabolic response to six dietary phases (5 d each), ranging from 50% surplus CHO (+50% CHO) to 50% deficient CHO (-50% CHO), and 50% surplus fat (+50% fat). 

A dose response was observed in glucose production with increasing carbohydrate intake, which stimulated moderate hyperinsulinemia and decreased lipolysis and fatty acid availability. The net effect was to increase glycogen stores and deliver extracellular glucose, thus favoring increased carbohydrate oxidation and a reciprocal decrease in fat oxidation (10).

Carbohydrate disposal is not different between glucose, fructose, and sucrose, in lean and obese women (11). Different carbohydrates behave in an essentially identical manner. A 50% overfeeding with either glucose, fructose and sucrose resulted in no significant difference in fat balance, and there were no significant differences between lean and obese women in macronutrient oxidation or balances. As expected, carbohydrate oxidation increased greatly in response to carbohydrate overfeeding (from 15.61 to 21.94, 21.64, and 21.97 MJ for fructose, glucose, and sucrose, respectively).

Of the excess carbohydrate, +74 % was oxidized (compared to only 18% of the excess fat intake) and on average 12% of the excess energy was stored as glycogen and 88% as fat; there was no significant difference between overfeeding treatments.

As seen in other studies (4,12), almost all of the glycogen storage occurred on day 1, with minimal imbalance on subsequent days, which may suggest the need for glycogen stores to first be perturbed to generate feedback control.

The daily carbohydrate imbalance with sucrose overfeeding asymptotically approached zero as carbohydrate oxidation gradually increased until it exactly matched intake. This caused glycogen storage to plateau at a new level ~110 g above the initial value.

Glycogen must be regulated within a relatively narrow window, and adipose tissue has evolved as the main energy storage compartment. Once any short-term changes in glycogen have resolved, additional energy excess or positive imbalances are buffered by fat stores. 

Carbohydrate vs. Protein

It was once thought that the auto-regulatory control of protein oxidation was as efficient as that of carbohydrate (13). However, a 160% increase in protein intake (from 47 g/d during underfeeding to 122 g/d during overfeeding) only caused a 12% increase in protein oxidation (from 83 g/d during underfeeding to 93 g/d during overfeeding) (4). 

In contrast, a 550% increase in carbohydrate intake (from 83 g/d during underfeeding to 539 g/d during overfeeding) was almost matched by a 420% increase in oxidation (from 106 g/d during underfeeding to 551 g/d during overfeeding). Carbohydrate was much more responsive, and it certainly exerted a much greater influence on the reciprocal changes in fat utilization than did protein (4). Protein takes a subordinate position to carbohydrate in terms of oxidation.

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