Carbohydrates make us fat. Seems like this shouldn’t be a controversial point, but it is in some areas. This study on carbohydrate overfeeding fed people 2.5 times their energy expenditure as carbohydrates (Aarsland A, Chinkes D, Wolfe RR. Hepatic and whole-body fat synthesis in humans during carbohydrate overfeeding. Am J Clin Nutr. 1997 Jun;65(6):1774-82).
We conclude that the liver plays a quantitatively minor role when surplus carbohydrate energy is converted into fat in the human body. The main site for fat synthesis is likely to be the adipose tissue.
Here’s the details of the study:
The respiratory exchange ratio (RER) was 0.81 +/- 0.01 in the basal state and 0.99 +/- 0.025 and 1.15 +/- 0.022 on days 1 and 4, respectively.
Although there was net fat oxidation in the basal state (955 +/- 139 mg.kg-1.min-1), there was net fat synthesis at the whole-body level both during early (day 1; 481 +/- 205 mg.kg-1.min-1) and late (day 4; 2243 +/- 253 mg.kg-1.min-1) carbohydrate overfeeding.
Although hepatic secretion of fat synthesized de novo increased approximately 35-fold during the study (basal state, 1.0 +/- 0.3; day 1, 13.8 +/- 6.8; and day 4, 43.3 +/- 16.3 mg.kg-1.min-1) this could only account for a small portion of total fat synthesis.
In the detailed study itself:
After 4 d of high-carbohydrate feeding, net fat synthesis at the whole body level was ~2250 mg /kg /d (ie, ~170 g/d). Thus, adaptation to a hyperenergetic carbohydrate diet involved a substantial increase in de novo lipid biosynthetic activity. However, at this time the liver produced ~40 mg fat – kg – d ‘ (ie, ~3 g/d). Although this value was 50-fold greater than the basal rate, hepatic de novo synthesis of fat only accounted for 2% of whole-body fat synthesis after 4 d of hyperenergetic carbohydrate feeding. Most likely, the adipose tissue had adapted to the high carbohydrate load by synthesizing 167 g fat/d.
This study puts it nicely (Flatt JP. Use and storage of carbohydrate and fat. Am J Clin Nutr. 1995 Apr;61(4 Suppl):952S-959S).
The body’s glycogen stores are so small that regulatory mechanisms capable of efficiently adjusting carbohydrate oxidation to carbohydrate intake have developed through evolution.
Fat oxidation is regulated primarily by events pertaining to the body’s carbohydrate economy, rather than by fat intake. Adjustment of fat oxidation to intake occurs because cumulative errors in the fat balance lead oven time to changes in adipose tissue mass, which can substantially alter free fatty acid concentration, insulin sensitivity, and fat oxidation. Fat intake and habitual glycogen concentnations are important in determining how fat one has to be to oxidize as much fat as one eats.
Flipping the coin the other way when you stop eating you burn through your body’s carbohydrate stores (Glycogen) and then your body starts burning its own fat. Also, the study notes:
Because the fraction of total dietary energy provided by protein is relatively small and relatively constant, and because the body spontaneously maintains a nearly constant protein content by adjusting amino acid oxidation to amino acid intake, body weight maintenance is primarily determined by the intake and utilization of carbohydrate and fat.
Continuing with the study:
Glucose uptake and glycogen synthesis are greatly stimulated by insulin, the secretion of which increases when blood glucose concentrations rise.
Note that when you are oxidizing carbohydrates you are not burning fat and the concentration of Insulin seems to be an important part of that switch. The glycogen storage process is fairly efficient:
Two moles ATP are expended to incorporate 1 mol glucose into glycogen. Because 36 ATP are gained during the complete oxidation of one molecule of glucose, 2/36, or ~5% of the energy content of glucose must be expended to store it as glycogen.
Glycogen storage fits the bill as the storage element for short term requirements.
The energy density of glycogen stores is thus only 4.2 kJ/g (~1 kcal/g), imposing definite limits on the amount of energy that can conveniently be carried in the form of glycogen.
Glycogen concentrations are highest in the liver, ie, typically ~4% after an overnight fast, and up to 8% after meals. Because an adult’s liver weighs ~1.5 kg, hepatic glycogen storage capacity is limited to ~120 g. Glycogen amounts in muscle are much lower and deliberate carbohydrate loading is necessary to raise them much above 2%. However, because muscle accounts for 20-30% of total body weight, the amount of glycogen stored in muscle is generally three to four times that in the liver. Total glycogen stones in adults can thus be estimated to be ~200-500 g, depending on body size and on the amount of carbohydrate consumed, and vary substantially during the day as a function of food intake and exertion.
The body’s glycogen reserve is in effect not much greater than the amount of carbohydrate usually consumed in 1 d, and maintenance of glycogen amounts within a desirable range requires effective adjustment of carbohydrate oxidation to carbohydrate intake.
Fat stands in contrast to glycogen stores which only store 1 kcal per gram (3/4 of the weight is water). Fat is stored without water and is stored at about 8 kcal per gram.
Thus, unusually large, occasional carbohydrate loads are
handled primarily by converting the absorbed glucose into
glycogen.
The following explains the details of the conversion of carbohydrates to fat.
The massive expansion of the glycogen stores then leads to the nearly exclusive use of glucose as a fuel (as shown in Figure 1 by the fact that the RQ remains close to 1.0 for many hours), in time reducing such temporary accumulations of glycogen. To induce substantial rates of carbohydrate conversion into fat, the body’s total glycogen stores must be considerably raised, from their usual 4-6 g/kg body wt to > 8-10 g/kg body wt. This requires deliberate and sustained ovenconsumption of large amounts of carbohydrates for ~2-3 d.
Fat gets handled differently in that it gets stored. When we eat fat we don’t burn more fat. Fortunately this is the case since we’d be in real trouble on a low carbohydrate diet since we don’t have the large amount of glycogen stores as our dietary buffers as someone who eats (buffers) a lot of carbohydrates.
…fat ingestion has so little effect on postprandial substrate oxidation is imputable to the relatively slow rate of fat absorption from the gut and to the fact that dietary fat is converted into chylomicrons targeted for deposition in adipocytes, allowing only a small fraction to reach other cells in the form of free fatty acids.
Thus, although carbohydrate intake has a powerful effect in promoting carbohydrate oxidation, ingestion of fat promotes fat oxidation only marginally, so that even the consumption of high fat meals leads to inhibition of fat oxidation during the following hours.
Eat more fat, burn less body fat.
