Effects of Carnitine Supplementation on Liver and Muscle

Not Applicable

Completed

• Conditions: Non-Alcoholic Fatty Liver Disease; Insulin Resistance
• Interventions: Dietary Supplement: Meal Replacement Drink; Dietary Supplement: L-Carnitine tartrate; Dietary Supplement: Maltodextrin

• Registration Number: NCT03439917
• Lead Sponsor: University of Nottingham

Brief Summary

It will be evaluated whether carnitine, a dietary supplement, reduces liver fat and improves metabolism in individuals who have a high concentration of fat within their liver. Participants will be given either Carnitine or placebo, together with a meal replacement milkshake twice daily for 6 months.

Detailed Description

NAFLD occurs when too much fat accumulates in liver tissue. This can, over time, cause inflammation and scarring of the liver, eventually leading to chronic liver disease and cirrhosis. It is strongly associated with diabetes and obesity, both of which are endemic in Western societies.

Carnitine enables cells in the body to use fat as a fuel, and recent studies have suggested that carnitine supplementation may reduce liver triglyceride content. Muscle and liver are the major sites in the body which coordinate glucose and fat metabolism. As well as assessing the effect of carnitine supplementation on liver fat, its effect on metabolic processes within these tissues will also be measured

Study Timeline

• Study First Submitted: 2018-02-14
• Study First Submitted QC: 2018-02-14
• Study First Posted: 2018-02-20
• Study Start: 2018-04-02
• Primary Completion: 2020-08-30
• Status Verified: 2021-11
• Study Completion: 2021-11-01
• Last Update Submitted: 2021-11-29
• Last Update Posted: 2021-11-30

Recruitment & Eligibility

• Status: COMPLETED
• Sex: Male
• Target Recruitment: 30

Inclusion Criteria

• Elevated liver fat on screening abdominal ultrasound
• Capable of providing informed consent
• Non-vegetarian diet
• BMI <40 kg/m2
• Weekly ethanol consumption <21 units/week
• Negative non-invasive liver screen, including Hepatitis B and C serology, liver autoantibodies, transferrin saturation, α1-antitrypsin levels.

Exclusion Criteria

• Known history of cardiovascular disease
• Known diabetes mellitus
• Known psychiatric comorbidity
• Chronic kidney disease
• Surgery within 6 months prior to start of study
• Exposure to drugs known to influence hepatic steatosis (including steroids, statins, omega-3-fatty acids)
• Current smokers
• Contraindications to magnetic resonance scanning, including implanted ferrous material (implantable pacemakers or defibrillators), metallic ocular foreign bodies, ferromagnetic aneurysm clips or severe claustrophobia.

Study & Design

• Study Type: INTERVENTIONAL
• Study Design: PARALLEL

Arm && Interventions

Group	Intervention	Description
Placebo and Meal Replacement Drink	Meal Replacement Drink	2g Maltodextrin consumed with a meal replacement milkshake (Slimfast, UK) twice a day for 24 weeks.
Carnitine and Meal Replacement Drink	L-Carnitine tartrate	2g L-carnitine tartrate consumed with a meal replacement milkshake (Slimfast, UK) twice a day for 24 weeks.
Carnitine and Meal Replacement Drink	Meal Replacement Drink	2g L-carnitine tartrate consumed with a meal replacement milkshake (Slimfast, UK) twice a day for 24 weeks.
Placebo and Meal Replacement Drink	Maltodextrin	2g Maltodextrin consumed with a meal replacement milkshake (Slimfast, UK) twice a day for 24 weeks.

Primary Outcome Measures

Name	Time	Method
Intrahepatic triglyceride (IHTG) content	24 weeks	IHTG measured by proton magnetic resonance spectroscopy

Secondary Outcome Measures

Name	Time	Method
Muscle lipid content	24 weeks	lipid content of the vastus lateralis muscle measured by proton magnetic resonance spectroscopy
whole body composition	24 weeks	Fat and lean tissue mass assessment by dual energy X-ray absorptiometry
liver sensitivity to insulin	24 weeks	suppression of glucose output from the liver during a 20 mU.m-2.min-1 hyperinsulinaemic euglycaemic clamp
whole body insulin sensitivity	24 weeks	whole body glucose uptake during a 50 mU.m-2.min-1 hyperinsulinaemic euglycaemic clamp
Liver energy metabolism	24 weeks	hepatic ATP flux assessed by 31-phosphorous magnetic resonance spectroscopy
Skeletal muscle sensitivity to insulin	24 weeks	Arterialised-venous vs. femoral venous difference in blood glucose concentration during the last hour of a 2 hour 50 mU.m-2.min-1 hyperinsulinaemic euglycaemic clamp

Trial Locations

Locations (1)

David Greenfield Human Physiology Unit; 🇬🇧 Nottingham, Notts, United Kingdom