35Non-Alcoholic Fatty Liver Disease (NAFLD) is associated with multi-organ (hepatic, skeletal muscle, 36 adipose tissue) insulin resistance (IR). Exercise is an effective treatment for lowering liver fat but its 37 effect on insulin resistance in NAFLD is unknown. 38We aimed to determine whether supervised exercise in NAFLD would reduce liver fat and improve 51With exercise, peripheral insulin sensitivity significant increased (following high-dose insulin) despite 52 no significant change in hepatic glucose production (following low-dose insulin); no changes were 53 observed in the control group. 54Although supervised exercise effectively reduced liver fat, improving peripheral IR in NAFLD, the 55 reduction in liver fat was insufficient to improve hepatic IR.

Context Randomised controlled trials in non-alcoholic fatty liver disease (NAFLD) have shown that regular exercise, even without calorie restriction, reduces liver steatosis. A previous study has shown that 16 weeks supervised exercise training in NAFLD did not affect total VLDL kinetics. Objective:To determine the effect of exercise training on intrahepatocellular fat (IHCL) and the kinetics of large triglyceride-(TG)-rich VLDL 1 and smaller denser VLDL 2 which has a lower TG content.Design A 16 week randomised controlled trial. Patients 27 sedentary patients with NAFLD.Intervention Supervised exercise with moderate-intensity aerobic exercise or conventional lifestyle advice (control).Main outcome Very low density lipoprotein1 (VLDL 1 ) and VLDL 2 -TG and apolipoproteinB (apoB) kinetics investigated using stable isotopes before and after the intervention. Results:In the exercise group VO 2max increased by 31Ϯ6% (meanϮSEM) and IHCL decreased from 19.6% (14.8, 30.0) to 8.9% (5.4, 17.3) (median (IQR)) with no significant change in VO 2max or IHCL in the control group (change between groups pϽ0.001 and pϭ0.02, respectively). Exercise training increased VLDL 1 -TG and apoB fractional catabolic rates, a measure of clearance, (change between groups pϭ0.02 and pϭ0.01, respectively), and VLDL 1 -apoB production rate (change between groups pϭ0.006), with no change in VLDL 1 -TG production rate. Plasma TG did not change in either group. Conclusion:An increased clearance of VLDL 1 may contribute to the significant decrease in liver fat following 16 weeks of exercise in NAFLD. A longer duration or higher intensity exercise interventions may be needed to lower plasma TG and VLDL production rate.

No significant differences were noted.

Nonalcoholic fatty liver disease (NAFLD) is characterized by low-circulating concentration of high-density lipoprotein cholesterol (HDL-C) and raised triacylglycerol (TAG). Exercise reduces hepatic fat content, improves insulin resistance and increases clearance of very-low-density lipoprotein-1 (VLDL1). However, the effect of exercise on TAG and HDL-C metabolism is unknown. We randomized male participants to 16 wk of supervised, moderate-intensity aerobic exercise ( n = 15), or conventional lifestyle advice ( n = 12). Apolipoprotein A-I (apoA-I) and VLDL-TAG and apolipoprotein B (apoB) kinetics were investigated using stable isotopes (1-[13C]-leucine and 1,1,2,3,3-2H5 glycerol) pre- and postintervention. Participants underwent MRI/spectroscopy to assess changes in visceral fat. Results are means ± SD. At baseline, there were no differences between exercise and control groups for age (52.4 ± 7.5 vs. 52.8 ± 10.3 yr), body mass index (BMI: 31.6 ± 3.2 vs. 31.7 ± 3.6 kg/m2), and waist circumference (109.3 ± 7.5 vs. 110.0 ± 13.6 cm). Percentage of liver fat was 23.8 (interquartile range 9.8–32.5%). Exercise reduced body weight (101.3 ± 10.2 to 97.9 ± 12.2 kg; P < 0.001) and hepatic fat content [from 19.6%, interquartile range (IQR) 14.6–36.1% to 8.9% (4.4–17.8%); P = 0.001] and increased the fraction HDL-C concentration (measured following ultracentrifugation) and apoA-I pool size with no change in the control group. However, plasma and VLDL1-TAG concentrations and HDL-apoA-I fractional catabolic rate (FCR) and production rate (PR) did not change significantly with exercise. Both at baseline (all participants) and after exercise there was an inverse correlation between apoA-I pool size and VLDL-TAG and -apoB pool size. The modest effect of exercise on HDL metabolism may be explained by the lack of effect on plasma and VLDL1-TAG.

Oral rehabilitation of missing teeth in cleft patients has acceptable success rates. A two-stage approach is indicated; however, timing of implant placement in the grafted maxilla varies within existing protocols. This case highlights successful implant osseointegration and esthetic oral rehabilitation following placement of two implants at 5 months after maxillary grafting (alveolar bone grafting) with a corticocancellous block obtained from the iliac crest. A 31-year-old male patient had already undergone repair of his bilateral cleft lip and soft palate according to established guidelines for cleft patients. Initial closure of his alveolar clefts and further correction of the maxillary hypoplasia with a bi-maxillary osteotomy were completed in 2002. However, bone resorption due to infection in 2003 necessitated removal of all maxillary incisors. The patient was not satisfied with the removable partial denture provided. In 2007, he did undergo anterior maxillary augmentation under general anesthesia, and 5 months later two implants were placed. A 3-unit bridge did replace functional and esthetic demands. Postoperative recovery was uneventful, and overall bone loss, and oral health remain within standards 28 months following implant placement. Optimal outcome is achievable when replacing missing teeth in cleft patients when timing does not exceed approximately a 6-month interval from bone grafting to implant placement. This article demonstrates that overall esthetic and functional rehabilitation is feasible in cleft lip and palate patients. In this patient, overall oral treatment was achieved with an implant prosthesis.