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I. Core Foundation:
1. GLP-1 receptor pathway (distributed throughout the body in multiple organs: brain, stomach, pancreas, liver)
Simulates the intestinal incretin GLP-1 secreted by the human intestine, responsible for controlling calorie intake and maintaining stable blood sugar:
- Hypothalamic appetite center: inhibits hunger signals, amplifies satiety signals;
- Gastrointestinal tract: slows down gastric emptying speed, prolongs the duration of satiety;
- Pancreatic β cells: glucose-dependent secretion, lowers blood sugar when it is high, automatically weakens when blood sugar is low, rarely causes hypoglycemia;
- Pancreatic α cells: inhibits excessive secretion of glucagon, reduces abnormal sugar production by the liver;
- Mildly regulates liver and fat metabolism, assisting in reducing lipid accumulation.
2. Glucagon receptor (GCGR) pathway (highly expressed in liver, white/brown fat)
This is the "fat-burning engine" lacking in single-target GLP-1 drugs, responsible for enhancing metabolism and breaking down fat:
- Liver cells: significantly activates fat β-oxidation and glycogen breakdown, forcibly mobilizing liver and visceral fat for energy supply;
- Fat tissue: stimulates lipolysis, breaks down triglycerides and releases free fatty acids;
- Whole-body thermogenesis: increases the resting basal metabolic rate, passively increasing total daily calorie consumption;
- Does not increase the risk of blood sugar elevation: The GLP-1 pathway counteracts the potential blood sugar-raising effect of GCGR, achieving a two-way balance of blood sugar homeostasis.
3. Dual receptor synergy logic
GLP-1 regulates less intake (throttling), GCGR regulates more burning (opening up resources), the two pathways do not cancel each other out but mutually enhance each other:
Single GLP-1 only reduces food intake, but the basal metabolism is likely to decrease with weight loss; combined with GCGR, metabolism does not decline, fat loss efficiency doubles, and targeted removal of visceral and liver ectopic fat is achieved.
II. Strong appetite suppression, prolonging satiety, reducing food intake at the source (GLP-1 dominant, GCGR assisting)
1. Central inhibition of appetite (brain hypothalamus)
Activates the satiety center in the arcuate nucleus of the hypothalamus and inhibits the hunger center:
- Reduces the craving for high-calorie, sweet foods, snacks, and lowers the desire for binge eating;
- Reduces the secretion of ghrelin (hunger hormone), enhances leptin sensitivity, and long-term improves the tendency to be hungry.
2. Peripheral prolongation of satiety (gastrointestinal tract)
- Prolongs gastric emptying: food stays in the stomach for a significantly longer time, a small amount of food produces a strong feeling of fullness;
- Slows down intestinal peristalsis, reduces rapid hunger after meals;
- Reduces gastric acid secretion after meals, reduces the urge to eat.
3. GCGR assists in consolidating the control of food intake
After GCGR activation, fat continues to break down for energy supply, the body is less likely to quickly experience hunger, significantly reducing the impulse for nocturnal and pre-meal binge eating.
III. Enhance liver fat breakdown, increase total daily calorie consumption (GCGR core function, GLP-1 enhancing effect)
(1) Liver: Strongly breaks down liver fat, reversing the core pathway of fatty liver
1. Activates liver cells' GCGR, increases intracellular cAMP, initiates fat acid β-oxidation: directly breaks down the accumulated triglycerides in liver cells, reduces lipid droplet deposition;
2. Inhibits liver fat from de novo synthesis (DNL): blocks the conversion of sugar to liver fat, reducing the progression of fatty liver from the source;
3. Promotes the outward transport of liver lipids: transports liver fat to systemic tissues for oxidation for energy supply, reduces the degree of liver fat infiltration;
4. Reduces liver inflammation: after the accumulation of fat decreases, the inflammation of liver lobules and ballooning degeneration of liver cells are simultaneously alleviated, improving metabolic-related fatty liver (MASLD) and even early fatty liver inflammation (MASH).
(2) Total calorie consumption increase (passive fat burning, not dependent on exercise)
1. Increases resting basal metabolism: GCGR stimulates liver heat production and activates brown fat heat production, calorie consumption during rest is significantly higher than simple dieting/single-target GLP-1; 2. Continuously mobilize internal visceral fat: Prioritize the breakdown of abdominal and visceral fat (the most harmful abdominal obesity fat) rather than simply subcutaneous water;
3. Reduce metabolic adaptation: During regular dieting for weight loss, the body automatically lowers metabolism to "save energy and survive", while the SUR10 GCGR pathway can counteract this metabolic decline, avoiding weight loss plateaus and rebounds.
IV. Losing fat while maximizing muscle retention, simultaneously improving fatty liver and glucose metabolism
1. Mechanism for fat loss and muscle preservation (distinguishing from regular dieting and partial weight loss drugs)
1. Energy supply prioritizes fat rather than muscle protein
The GCGR continuously mobilizes fat as the main energy source, and the body does not need to break down skeletal muscle protein for energy supply; when the calorie gap is large in simple dieting or partial weight loss plans, muscle will be lost simultaneously, and the basal metabolism decreases the more it is reduced.
2. GLP-1 pathway protects the muscle synthesis signal
Improving overall sensitivity is the key hormone for muscle protein synthesis; the glucose uptake of muscle cells increases, maintaining the rate of muscle protein synthesis, and reducing muscle loss.
3. Reduce inflammation and lower muscle breakdown factors
After reducing visceral fat, the low-grade chronic inflammation throughout the body is alleviated, and inflammatory factors will accelerate muscle breakdown; SUR10 reduces the level of inflammation and maintains muscle mass, resulting in a firm and non-sagging body shape after weight loss, and retaining the basal metabolism.
2. Complete improvement chain for fatty liver (MASLD/MASH)
1. Short term: Rapidly reduce the triglyceride content in the liver, reduce liver fat infiltration;
2. Mid term: Alleviate hepatic steatosis, reduce liver inflammatory infiltration;
3. Long term: Improve liver resistance, break the vicious cycle of "fat accumulation → insulin resistance → more fat deposition";
Hong Kong Biopetide Research Limited is a high-tech enterprise specializing in the research, development, production, and sales of peptide products. The company boasts advanced laboratories and a rigorous quality control system, with its products having obtained multiple international certifications, ensuring safety and efficacy.
Its customers are spread across Europe, the United States, Southeast Asia, the Middle East, and other regions.
Biotechnology Co., Ltd. is a high-tech enterprise specializing in the research, development, production, and sales of peptide products. With advanced laboratories and a rigorous quality control system, our products have obtained international certification, ensuring safety and efficacy.
As a global trading company, we provide customized solutions to customers across Europe, the United States, Southeast Asia, the Middle East, and many other regions. Upholding the philosophy of "technology leading health," we are committed to innovation, striving to deliver high-quality health products to consumers worldwide. Our business principles focus on establishing a strong domestic market presence, increasing R&D investment, manufacturing premium products, and leveraging technology to promote environmental protection and sustainable development. At the same time, we actively expand into international markets, serve society with sincerity, and aim to become a modern, eco-friendly, and technologically advanced enterprise that meets global standards. Contact Us
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