Abstract
(1) Background. Multiple sclerosis (MS) is characterised by the loss of muscle throughout the course of the disease, which in many cases is accompanied by obesity and related to inflammation. Nonetheless, consuming epigallocatechin gallate (EGCG) and ketone bodies (especially β-hydroxybutyrate (βHB)) produced after metabolising coconut oil, have exhibited anti-inflammatory effects and a decrease in body fat. In addition, butyrylcholinesterase (BuChE), seems to be related to the pathogenesis of the disease associated with inflammation, and serum concentrations have been related to lipid metabolism. Objective. The aim of the study was to determine the role of BuChE in the changes caused after treatment with EGCG and ketone bodies on the levels of body fat and inflammation state in MS patients. (2) Methods. A pilot study was conducted for 4 months with 51 MS patients who were randomly divided into an intervention group and a control group. The intervention group received 800 mg of EGCG and 60 mL of coconut oil, and the control group was prescribed a placebo. Fat percentage and concentrations of the butyrylcholinesterase enzyme (BuChE), paraoxonase 1 (PON1) activity, triglycerides, interleukin 6 (IL-6), albumin and βHB in serum were measured. (3) Results. The intervention group exhibited significant decreases in IL-6 and fat percentage and significant increases in BuChE, βHB, PON1, albumin and functional capacity (determined by the Expanded Disability Status Scale (EDSS)). On the other hand, the control group only exhibited a decrease in IL-6. After the intervention, BuChE was positively correlated with the activity of PON1, fat percentage and triglycerides in the intervention group, whereas these correlations were not observed in the control group (4). Conclusions. BuChE seems to have an important role in lipolytic activity and the inflammation state in MS patients, evidenced after administering EGCG and coconut oil as a βHB source.
Highlights
Multiple sclerosis (MS) is an autoimmune disease that produces demyelination on the sheath of neurons
The main characteristic is chronic inflammation that causes a gradual increase in oxidative stress [6,7,8], which contributes to increased inflammation demyelination and neurodegeneration [7,8]
An increase in body fat is associated with a greater expression of the butyrylcholinesterase enzyme (BuChE) in blood serum [15]
Summary
Multiple sclerosis (MS) is an autoimmune disease that produces demyelination on the sheath of neurons. There are different types of the disease, the majority are relapsing–remitting multiple sclerosis (RRMS) that can evolve into secondary progressive multiple sclerosis (SPMS) [1,2,3]. There are several physical consequences, including anthropometric changes in patients as the disease progresses, characterised by the loss of lean mass [9,10]. The loss of muscle is directly associated with an increase in body fat in MS patients [11]. This causes a rise in inflammation [12], resulting in a loss in respiratory capacity and fatigue [13]; the patient’s disability and the progression of the disease are increased [14]. An increase in body fat is associated with a greater expression of the butyrylcholinesterase enzyme (BuChE) in blood serum [15]
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