|dc.contributor.author||Craig, Thomas P.||-|
|dc.description.abstract||L- Carnitine is a vitamin like compound synthesised endogenously from the essential amino acids methionine and lysine and plays an essential role in the metabolism of fatty acids. Beta-oxidation, the major process by which long chain fatty acids are oxidised in mitochondria, depends on carnitine. In theory, increased carnitine availability could increase the ability to transport long chain fatty acids into the mitochondria and thus increase their oxidation.
Recent work has however shown that it is unlikely that carnitine supplementation will increase fat oxidation and may instead promote carbohydrate metabolism. Researched elements have included the role carnitine may play in muscle glycogen storage, carnitine as a potential preventative mechanism for clinical populations at risk from metabolic disorders and “insulin like” effects observed in carnitine trials.
This study examined the effects of 14 days L-Carnitine L-Tartrate (LC) supplementation on blood glucose and insulin response to an oral glucose tolerance (OGTT) test and submaximal exercise. Sixteen male participants were recruited and assigned to two groups (lean (n=8) and overweight/obese (n=8)). After completing a first visit for a submaximal predictive exercise test, participants attended on three further occasions, in the morning after an overnight fast, for fasting blood samples and 2hr OGTT tests followed by an exercise bout (20 min at 40% of predicted VO2peak).
The first test was a familiarisation trial and the final two tests were conducted two weeks apart following 14 days of ingestion of placebo (PL, 3g glucose/day) or LC (3g/day) ingested as 2 capsules 3x/day with meals. Blood was drawn at rest and at 15, 30, 45, 60, 90, and 120 minutes of OGTT and at 10 and 20 min of exercise for analysis of glucose and insulin. Data obtained were then used for determination of usual insulin sensitivity indices (HOMA-IR, Area Under Curve (AUC) glucose, AUC insulin, 1st phase and 2nd phase beta cell function, estimated insulin sensitivity index, and estimated metabolic clearance rate).
There was a significant difference between groups for body mass, % fat and BMI with no significant difference in age and height. Mean fasting glucose (5.4(0.2) Placebo (PL); 5.5(0.2) L-Carnitine (LC); mmol/L), insulin (13.7(3.5) PL; 13.7(4.2) LC; muU/ml) and HOMA-IR (2.6(0.6) PL; 2.7(0.4) LC) were not different between trials, and no significant differences were observed between groups prior to supplementation. Analysis of the blood glucose response during the OGTT revealed no group effect but there was a time effect (P<0.01) and a trial x time interaction (p<0.01).
Highest plasma glucose concentration was observed at 30 minutes in both trials but was significantly lower (p<0.05) at 30 min in the trial after LC (8.55(0.44) PL; 7.34(0.36) LC; mmol/L). AUC glucose was not different between trials but AUC insulin tended to be higher following LC (5029(889) PL; 5845(1032) LC, p=0.09). Estimated 1st phase (281(64) PL; 419(38) LC; muU/ml) and 2nd phase (106(12) PL; 132(8) LC; muU/ml) beta-cell function were both significantly (p<0.05) greater following LC supplementation.
No treatment differences were observed in glucose and insulin response to exercise but a trial by group interaction revealed that plasma glucose was lower after 10 minutes in the lean group (p<0.05) and plasma insulin higher at 20 minutes of exercise in the overweight/obese group (p<0.05). No effects of LC supplementation were observed on heart rate, VO2 or Respiratory Exchange Ration (RER) during the exercise task.
It is concluded that LC appears to induce changes in blood glucose regulation during an OGTT, that this may be driven by changes in beta-cell function or in incretin levels, with Glucagon Like Peptide-1 (GLP-1) of particular interest, and that this response to LC supplementation is not different between lean and overweight/obese but may be related to aerobic capacity. Muscle glycogen levels focusing on an elite athlete population are also of interest.
Therefore, further investigation of carnitine action on beta-cell function, incretin and muscle glycogen level is warranted.||en_GB|
|dc.publisher||University of Stirling||en_GB|
|dc.subject||Oral Gluocal Tolerance||en_GB|
|dc.subject||Type 2 diabetes||en_GB|
|dc.subject.lcsh||Athletic Performance physiology||en_GB|
|dc.title||Dietary Carnitine Supplementation as a potential modulator of insulin sensitivity||en_GB|
|dc.type||Thesis or Dissertation||en_GB|
|dc.type.qualificationname||Master of Philosophy||en_GB|
|dc.contributor.affiliation||School of Sport||en_GB|
|Appears in Collections:||Faculty of Health Sciences and Sport eTheses|