WO-2026095764-A1 - COMPOSITION FOR REGULATING HEPATIC LIPID METABOLISM, COMPRISING LACTIPLANTIBACILLUS PLANTARUM OPT-A1 STRAIN

WO2026095764A1WO 2026095764 A1WO2026095764 A1WO 2026095764A1WO-2026095764-A1

Abstract

The present invention relates to a composition for regulating hepatic lipid metabolism, comprising Lactiplantibacillus plantarum OPT-A1 strain deposited under accession number KCTC 15555BP, a culture liquid thereof, a cultured product thereof, or a culture lysate thereof. The composition suppresses lipid accumulation and expression of genes related to lipogenesis in hepatocytes, and enhances expression of genes related to lipid oxidation. In addition, the composition inhibits accumulation of triglycerides in hepatocytes and reduces blood triglyceride levels, total cholesterol levels, and liver injury indices. Furthermore, the composition promotes rapid consumption of lipids in hepatocytes and somatic cells through enhancement of muscle mass, and thus can be advantageously used as a raw material for foods, pharmaceuticals, and the like related to alleviation and treatment of various metabolic diseases.

Inventors

CHA, HOON
KWON, SOON HYUN
CHEONG, KWANG HO
KIM, SUN KYU
CHOI, WOO JIN
CHOI, Bo Bin
JUN, HYEON
KWON, GYEONG YEOL
LEE, SEUNG HEON
KIM, EO JIN

Assignees

(주) 옵트바이오

Dates

Publication Date: 20260507
Application Date: 20251002
Priority Date: 20241030

Claims (14)

A composition for regulating liver lipid metabolism characterized by comprising the Lactiplantibacillus plantarum OPT-A1 strain deposited at KCTC15555BP, the culture medium thereof, the culture thereof, or the culture lysate thereof.
In paragraph 1, The above composition is a composition for regulating liver lipid metabolism, characterized by inhibiting lipid accumulation within liver cells.
In paragraph 1, The above composition is a composition for regulating liver lipid metabolism characterized by having the efficacy of activating AMPK (AMP-activated protein kinase) in liver cells.
In paragraph 1, The above composition is a composition for regulating liver fat metabolism characterized by inhibiting the accumulation of triglycerides in liver cells.
In paragraph 1, The above composition is a composition for regulating liver fat metabolism characterized by reducing the production of blood triglycerides, total cholesterol, AST (Aspartate aminotransferase), and ALT (Alanine aminotransferase).
In paragraph 1, The above composition is a composition for regulating liver fat metabolism characterized by increasing the production of adiponectin, a fat-degrading hormone.
In paragraph 1, The above composition is a composition for regulating liver lipid metabolism characterized by inhibiting the expression of fat synthesis-related genes, such as FAT/CD36 (Fatty acid translocase), PPARγ (Peroxisome proliferator-activated receptor-γ), or FAS (Fatty acid synthase).
In paragraph 1, The above composition is a composition for regulating liver lipid metabolism characterized by enhancing the expression of fatty acid oxidation-related genes, PPAR-α (Peroxidase proliferator-activated receptor-α) and CPT1 (Carnitine palmitoyltransferase 1).
In paragraph 1, The above composition is Escherichia coli or Klebsiella pneumoniae that induce fatty liver formation. A composition for regulating liver lipid metabolism characterized by having antibacterial activity against pneumoniae .
In paragraph 1, A composition for regulating liver lipid metabolism characterized by activating GLP-1 (glucagon-like peptide-1).
In paragraph 1, The above composition is a composition for regulating liver fat metabolism characterized by having muscle-increasing efficacy.
A pharmaceutical composition for the prevention or treatment of fatty liver, characterized by comprising the composition of claim 1.
A food composition for the prevention or improvement of fatty liver, characterized by comprising the composition of claim 1.
A method for treating fatty liver using the Lactiplantibacillus plantarum OPT-A1 strain deposited at KCTC15555BP, its culture medium, its culture, or its culture lysate.

Description

Composition for regulating liver lipid metabolism comprising the Lactiplantibacillus plantarum OPT-A1 strain The present invention relates to Lactiplantibacillus plantarum deposited as KCTC15555BP, which has AMPK (AMP-activated protein kinase) and GLP-1 (glucagon-like peptide-1) activating efficacy. The present invention relates to a composition for regulating liver lipid metabolism comprising the OPT-A1 strain ( plantarum ) OPT-A1, the culture medium thereof, the culture thereof, or the culture lysate thereof. The World Health Organization (WHO) defines obesity as 'a condition in which abnormal or excessive fat is accumulated in adipose tissue to the extent that it is detrimental to health.' Recently, it has been reported that the proportion of the world's overweight population will steadily increase from 38% in 2020 to 42% in 2025, 46% in 2030, and 51% in 2035, while the proportion of the obese population will steadily increase from 14% in 2020 to 17% in 2025, 20% in 2030, and 24% in 2035. With industrialization, modern people have increasingly adopted high-fat, high-salt, high-sugar, and high-calorie diets resulting from the consumption of meat-centered saturated and unsaturated fatty acids, sodium, and sugars. Consequently, metabolic diseases caused by overweight are on the rise, including Type 2 diabetes, dyslipidemia, hypertension, fatty liver, gallbladder disease, coronary artery disease (angina, myocardial infarction), stroke, sleep apnea, gout, osteoarthritis, menstrual irregularities, colorectal cancer, and breast cancer. Furthermore, irregular eating habits not only lead to poor nutritional status but can also cause psychological and physiological unhealthiness and variability. Therefore, it is advisable to prevent obesity in advance; if obesity occurs, regulating metabolism through body fat reduction to ensure smooth functioning is crucial for preventing various diseases and maintaining health. AMPK (adenosine monophosphate-activated protein kinase) is a kinase that regulates energy status sensing and metabolic homeostasis in tissues such as fat, liver, pancreas, and muscle. AMPK activation is an important target substance for preventing and treating metabolic diseases because it reduces triglyceride accumulation in adipose tissue by increasing fatty acid oxidation—specifically mitochondrial beta-oxidation—and inhibiting fat synthesis. Under conditions of overnutrition, adipocytes store triglycerides in the form of fatty acids, which consist of three fatty acids linked to a glycerol core; the continuous accumulation of triglycerides leads to hypertrophy of these cells. Hypertrophied adipocytes are associated with metabolic disorders, including insulin resistance, circulatory disorders, and inflammation. Sterol regulatory element binding proteins-1c (SREBP-1c) increases the synthesis of fatty acids and triglycerides within adipocytes, leading to their accumulation, by regulating the expression of C/EBP-α (CCAAT/enhancer binding protein-α), peroxidase proliferator-activated receptor-γ (PPAR-γ), and fatty acid synthase (FAS). During the early stages of adipocyte differentiation, the expression of C/EBP-α increases, as does the expression of PPAR-γ, a late-stage transcription factor and differentiation regulatory transcription factor. This leads to the activation of lipid synthesis genes and the regulation and promotion of differentiation, thereby completing the process of adipocyte formation and differentiation. To regulate lipid synthesis, AMPK is activated to suppress the expression of lipid synthesis genes. Additionally, it oxidizes lipids by increasing mitochondrial beta-oxidation through the activation of peroxidase proliferator-activated receptor-α (PPAR-α) and carnitine palmitoyltransferase 1 (CPT1). Uncoupling protein 1 (UCP1) is expressed during the oxidation of fatty acids, as it consumes energy in the mitochondria of adipocytes to generate heat as a byproduct. Accordingly, regulating various such factors, including AMPK, is becoming a target for suppressing obesity, and various studies are currently underway. GLP-1 (glucagon-like peptide-1), another obesity regulatory factor, is an incretin hormone that plays a role in lowering blood sugar by promoting insulin secretion and inhibiting glucagon secretion in a glucose concentration-dependent manner. Recently, GLP-1 has been approved as an obesity treatment and is one of the substances gaining attention as an obesity treatment. GLP-1 secreted from the intestines exerts efficacy on various metabolic diseases through the blood, including weight loss, blood sugar control, blood pressure reduction, lipid improvement, and fatty liver improvement. Meanwhile, among these obesity-related metabolic syndromes, the symptom that can appear most rapidly is non-alcoholic fatty liver disease; when excessive calories are continuously consumed, fat accumulates in the liver just as it accumulates in fat cells in the body. Fatty liver is diagnosed when excess