Irisin Myokine for Pancreatic Beta-Cell Preservation

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Solution Overview

Problem

Current treatments for type 2 diabetes mellitus, such as metformin, glitazones, and sulfonylureas, do not effectively protect pancreatic beta-cells from dysfunction and death, leading to inadequate insulin production and secretion, and are associated with significant side effects and healthcare costs.

Innovation Solution

The use of irisin, a myokine derived from skeletal muscle, to prevent the dysfunction and death of pancreatic beta-cells by promoting insulin synthesis, secretion, and proliferation, as well as reducing apoptosis induced by cytotoxic stimuli, particularly in conditions of metabolic stress like obesity.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Quantity of substance

If current diabetes treatments (metformin, glitazones, sulfonylureas) are used to control blood glucose levels, then glycemic control is improved, but pancreatic beta-cell protection is insufficient and side effects increase

Engineering Contradiction:

Improveblood glucose controlVSAvoidbeta-cell protection

Core Design Contradiction:

Quantity of substanceVSReliability

Solution Approach 1:

The patent introduces irisin as a mediatory substance that indirectly protects beta-cells by improving insulin sensitivity in peripheral tissues and reducing metabolic stress on the pancreas, rather than directly stimulating insulin secretion or affecting glucose levels alone

Inventive Principle:

Principle #24Intermediary (Mediator)

Solution Approach 2:

The patent converts the harmful effect of metabolic stress and insulin resistance into a beneficial therapeutic outcome by using irisin to improve insulin sensitivity, thereby reducing the metabolic burden on beta-cells and preventing their dysfunction

Inventive Principle:

Principle #22Blessing in disguise (Convert harm into benefit)

2Quantity of substance

If sulfonylureas are used to stimulate continuous insulin production, then blood glucose control is improved, but beta-cell survival is compromised and hypoglycemia risk increases

Engineering Contradiction:

Improveinsulin productionVSAvoidbeta-cell damage

Core Design Contradiction:

Quantity of substanceVSObject-affected harmful factors

Solution Approach 1:

Instead of stimulating beta-cells to overproduce insulin (which damages them), the patent uses irisin to improve peripheral insulin sensitivity, allowing the body to utilize existing insulin more effectively and reducing the need for excessive insulin production

Inventive Principle:

Principle #13The other way round (Inversion)

Solution Approach 2:

The patent enables the body's own insulin to work more effectively by improving insulin sensitivity through irisin, rather than forcing beta-cells to produce more insulin through pharmacological stimulation

Inventive Principle:

Principle #25Self-service

3Quantity of substance

If metformin is used to reduce hepatic glucose release, then blood glucose control is improved, but beta-cell protective effects are unclear and gastrointestinal side effects occur

Engineering Contradiction:

Improvehepatic glucose releaseVSAvoidgastrointestinal side effects

Core Design Contradiction:

Quantity of substanceVSObject-generated harmful factors

Solution Approach 1:

The patent uses irisin as a mediatory myokine that improves insulin sensitivity in multiple tissues including liver, muscle, and adipose tissue, providing a more comprehensive and physiologically natural approach compared to metformin's direct hepatic action

Inventive Principle:

Principle #24Intermediary (Mediator)

Data Source

PatentEP3373955B1Pharmacological use of an irisin in pancreas diseases or dysmetabolic conditions, wherein a pancreas damage occurs

Publication Date: 2022.01.12 UNIV DEGLI STUDI DI BARI

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Figure 3a~3b

AI summary

Object of the present invention is the use of a known protein, irisin, for preservation of the functionality and survival of the cells of the pancreatic islets.