Endocrine Abstracts

Moderate, ‘Atkin’s-style’ low-carbohydrate/high fat diets (LC-HFD) are claimed to induce weight loss in overweight subjects and to ameliorate glucose metabolism, whereas extreme ketogenic LC-HFD are used to treat neurological disorders like pediatric epilepsy. To investigate the effects of both types of LC-HFD on glucose and insulin metabolism independent of the energetic intake, we pair-fed male Wistar rats isoenergetic of standard rodent chow (CH) or one of two different LC-HF diets (percentage of metabolizable energy, fat/protein/CHO: LC-HF-1 (78.7/19.1/2.2), LC-HF-2 (92.8/5.5/1.7) and CH (16.7/19./64.3)) for 4 weeks. Since we had previously observed increased visceral fat accumulation in rats pair-fed the LC-HFD, we also studied rats in which the fat mass was clamped to the control group by restricting LC-HFD intake to 80% of caloric intake of the control group. In pair-fed groups, rats on LC-HFD displayed significantly higher fat mass when compared to CH (P<0.01). Furthermore, dynamic challenge tests (oGTT, i.p.GTT, insulin tolerance tests and hyperinsulinemic-euglycemic clamp) revealed that rats pair-fed the LC-HF diets have impaired glucose tolerance. As expected, the reduction of LC-HFD intake to only 80% equalized the fat mass between LC-HFD groups and controls. The restriction of LC-HFD intake to 80% improved glucose tolerance during oGTT compared to rats which were regularly pair-fed with LC-HFD. However, glucose tolerance was still impaired when compared to rats fed the standard control diet (AUC of glucose during oGTT: Chow: 12 986±801; LC-HF-1 (80%): 15 662±1111; LC-HF-2 (80%): 23 809±1485; CH vs LC-HF-1 (80%): P=0.087; CH vs LC-HF-2 (80%): P<0.001). In summary, these data clearly argue against a beneficial effect of LC-HFD on glucose and insulin metabolism. Impaired glucose tolerance occurred with LC-HFD independent of the relative abundance of fat and protein and in the absence, energy overconsumption and increased fat mass.