Endocrine Abstracts

Maintenance of ketosis and increases in resting energy expenditure (EE) are two proposed mechanisms for weight loss observed in humans performing low-carbohydrate/high-fat (LC-HF) diets like the Atkin’s diet. To explore these potential mechanisms, we pair-fed isocaloric amounts of regular chow (CH) or two LC-HF diets (carbohydrates~1%ME) to male Wistar rats for 4 weeks. LC-HF-1 (fat~66%ME) was matched in protein content to CH, whereas LC-HF-2 was even higher in fat (~94%ME). We analyzed bodyweight (BW) gain, EE, respiratory quotient (RQ), serum ketone-bodies (β-hydroxybutyrat, HBA), free fatty acids (FFA), urea, glucose and insulin. In addition, daily nitrogen balance and urinary energy contents were measured.

BW gain was slightly reduced in the LC-HF-1 group, and clearly reduced in LC-HF-2 (P<0.01). Animals on LC-HF-1 accumulated most nitrogen per day; LC-HF-2 the least. Furthermore, daily nitrogen balance was barely positive and serum urea considerably reduced in LC-HF-2. Remaining energy in urine was lower in LC-HF-2 when compared to CH (0.3±0.12 vs 0.93±0.23 KJ/g; P<0.01); overall 24-h loss was below 5 KJ in all groups. RQ was ~1 in CH and lower in LC-HF-1 (0.81±0.01) and LC-HF-2 (0.76±0.01, P<0.001). Of d24-h EE was significantly lower in both LC-HF groups. Only in LC-HF-2 concentrations of FFA (two-fold) and HBA (four-fold) were significantly increased.

In conclusion, LC-HF-2 diet induced ketosis, but did not increase EE or energy loss through urine. The impaired BW gain in this group was probably caused by the relative protein shortage and resulting inability to acquire muscle mass. Macronutrient composition of LC-HF-1 better reflects human LC-HF diets. Indeed, slight reductions in BW gain were seen. However, LC-HF1 neither induced ketosis nor increased EE. RQ data and unchanged glucose levels suggest presence of gluconeogenesis in this group. Our data in rats do not support the proposed mechanisms for weight loss in humans performing LC-HF diets.