2-Monoacylglycerol Degrading Enzyme for Reducing Blood Triglycerides
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Solution Overview
Problem
Current treatments for liver steatosis, non-alcoholic fatty liver, hyperlipidemia, type 2 diabetes, and obesity often come with side effects such as cardiovascular issues, central nervous system effects, and gastrointestinal discomfort, and existing drugs have limited efficacy and specificity, necessitating a more effective and side-effect-free therapeutic approach.
Innovation Solution
A method utilizing a 2-monoacylglycerol degrading enzyme that completely degrades triglycerides into fatty acids and glycerol in the digestive tract, delaying fat absorption and promoting energy consumption by delaying re-synthesis of triglycerides in digestive epithelial cells, thereby reducing blood triglyceride absorption and aiding in weight management.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If conventional drugs are used to treat liver steatosis, non-alcoholic fatty liver, hyperlipidemia, type 2 diabetes, and obesity, then therapeutic effects are achieved, but side effects such as cardiovascular issues, central nervous system effects, and gastrointestinal discomfort occur
Solution Approach 1:
The patent extracts and utilizes a specific enzyme (2-monoacylglycerol degrading enzyme) from the digestive system to target and degrade triglycerides specifically in the digestive tract, separating the therapeutic function from the harmful side effects of conventional systemic drugs. This localized enzymatic action treats metabolic diseases without affecting other body systems, thereby eliminating side effects while maintaining therapeutic efficacy.
2Quantity of substance
If existing drugs are used to suppress fat absorption, then fat absorption is reduced, but efficacy is limited and specificity is insufficient
Solution Approach 1:
The patent applies local quality by using a 2-monoacylglycerol degrading enzyme that specifically targets and degrades triglycerides at the 2-position of the glycerol backbone in the digestive tract. This positional specificity allows the enzyme to act selectively on triglycerides during digestion, providing both high efficacy in reducing fat absorption and high specificity in targeting the correct molecular structure, thereby resolving the contradiction between quantity reduction and reliability.
Applied Scientific Principles
This section explains which scientific principles are used to turn an abstract innovation direction into a practical engineering solution.
Function Achieved in This Case
The method effectively treats liver steatosis, non-alcoholic fatty liver, hyperlipidemia, and obesity by reducing fat absorption and increasing energy consumption, offering a safer and more sustainable treatment option compared to existing therapies.
Implementation Method 1
the 2-monoacylglycerol degrading enzyme completely degrades triglyceride into fatty acids and glycerol in a digestive tract
Implementation Method 2
recombination thereof into triglyceride in the digestive epithelial cells is delayed or energy consumption is promoted during this process
Data Source
AI summary
The present invention relates to a method for treating liver steatosis or non-alcoholic fatty liver by using a 2-monoacylglycerol degrading enzyme. More particularly, the present invention provides a method for treating metabolic syndrome such as liver steatosis, non-alcoholic fatty liver, hyperlipidemia, type 2 diabetes, and/or obesity by using a 2-monoacylglycerol degrading enzyme, in which the 2-monoacylglycerol degrading enzyme completely degrades triglyceride into fatty acids and glycerol in a digestive tract such that fat absorption is delayed and blood absorption of triglyceride is decreased, and in which, in a case where monoacylglycerol is degraded by a monoacylglycerol lipase in a digestive tract, although degraded products of the monoacylglycerol are absorbed into digestive epithelial cells, recombination thereof into triglyceride in the digestive epithelial cells is delayed or energy consumption is promoted during this process.