MCP for Three Highs

Low Molecular Weight Citrus Pectin, also known as Modified Citrus Pectin (MCP) or Low Molecular Citrus Pectin (LCP), is a galactose-rich, small-molecule, water-soluble dietary fiber polysaccharide extracted from the peel and inner membrane of citrus fruits (lemon, orange, mandarin, pomelo, etc.) using advanced biological enzymatic hydrolysis technology.

Zhejiang Gold Kropn Bio-tech Co., Ltd. has collaborated with Zhejiang University, Tianjin University, Fudan University, Xinxiang Medical University, and other institutions on research into MCP production processes and functional studies, and has been granted multiple national invention patents. Studies have shown that MCP of varying molecular weights and degrees of esterification can help boost human immunity, inhibit tumor cell activity, and help manage the "three highs," among other functions. The company is currently the only MCP manufacturer in Asia, and one of only two in the world.

1.1 Mechanism of MCP's lipid-lowering effect

Elevated blood lipids are characterized by increased serum triglycerides and cholesterol, and are among the risk factors for cardiovascular disease. Numerous studies in recent years have confirmed that MCP has a significant effect in lowering triglyceride and cholesterol levels in the human body, and may help protect against cardiovascular conditions such as atherosclerosis, hypertension, and coronary heart disease. MCP lowers only the low-density lipoprotein (LDL) and very-low-density lipoprotein (VLDL) cholesterol that are harmful to health, while high-density lipoprotein (HDL) cholesterol is unaffected by MCP.

Reducing intake of exogenous fat and energy MCP is not easily broken down in the upper gastrointestinal tract, and most of it is neither digested nor absorbed. Due to its water-holding capacity and macromolecular structure, it swells in the upper digestive tract after absorbing water, creating a feeling of fullness in the intestines. This increases satiety and slows gastric emptying, which in turn affects hormone secretion in response to meals, influences food intake, and reduces the intake of fat and energy.

Reducing absorption of endogenous lipids MCP reduces the absorption of endogenous lipids through several mechanisms, mainly the following six:

(1) Adsorption: MCP molecules contain ester groups, and their high viscosity and macromolecular structure allow chylomicron fat, cholesterol, and other lipid substances in the body to be adsorbed by the pectin and then excreted with stool, reducing the rate of dietary cholesterol absorption.

(2) Physical barrier effect: MCP binds with glycoproteins on the epithelial mucosal cells of the small intestine, forming a thickened, unstirred water layer that limits the rate of absorption. This acts as a physical barrier that directly impedes the diffusion of dietary cholesterol toward the mucosal cells of the intestinal wall, and interferes with the formation of fat micelles as well as the emulsification of bile and cholesterol, substantially interfering with the absorption of dietary cholesterol. In addition, water-soluble pectin is highly viscous and forms a gel-like solution upon absorbing water in the digestive tract; this gradually forms macromolecules that combine with chyme to create a large gel mass, increasing the viscosity of the chyme and reducing the rate at which cholesterol reaches the surface of the small intestinal mucosa, thereby lowering the cholesterol absorption rate.

(3) Effects on bile acid metabolism: MCP binds with cholesterol or bile acids, reducing the bile acids available for the synthesis of endogenous cholesterol, thereby reducing the reabsorption of cholesterol in the intestine and reducing enterohepatic circulation, while promoting its breakdown and excretion and impairing lipid emulsification. MCP also alters the number and activity of bacteria in the large intestine, speeding up intestinal transit and shortening the time food remains in the intestine, thereby accelerating bile acid excretion. The resulting reduction in bile acid levels promotes negative feedback on hepatic cholesterol synthesis, causing more cholesterol to be converted into bile acids and promoting bile acid excretion, which lowers plasma cholesterol and triglyceride levels - helping to prevent conditions such as atherosclerosis and coronary heart disease.

(4) Effects of colonic metabolites: MCP can be almost entirely fermented and broken down by bacteria in the large intestine, producing short-chain fatty acids (SCFAs) - mainly acetic acid, propionic acid, and butyric acid - as breakdown products. These short-chain fatty acids are fully absorbed in the human colon and influence the hepatic metabolism of cholesterol and bile acid absorption. Short-chain fatty acids bind with soluble calcium, which in turn affects the solubility of bile acids in the large intestine and thereby influences bile acid reabsorption. As a result, the degree to which pectin can be fermented in the lower intestinal tract correlates with the degree of cholesterol reduction. In addition, the production of short-chain fatty acids lowers colonic pH, which reduces bile acid solubility and passive reabsorption.

(5) Effects on key enzymes in cholesterol metabolism: Key enzymes involved in cholesterol metabolism include lecithin-cholesterol acyltransferase (LCAT), the key enzyme for cholesterol esterification and transport; lipoprotein lipase (LPL), the key enzyme for triglyceride breakdown; hepatic 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA reductase), the rate-limiting enzyme for hepatic cholesterol synthesis; and 7α-hydroxylase, the key enzyme for hepatic bile acid synthesis. Related research suggests that MCP enhances the activity of LCAT, LPL, HMG-CoA reductase, and 7α-hydroxylase, accelerating the further breakdown of cholesterol into bile acids, reducing cholesterol absorption, and reducing enterohepatic circulation of bile acids, resulting in lower plasma cholesterol levels. However, hepatic HMG-CoA reductase and 7α-hydroxylase are also directly regulated at the cellular level by short-chain fatty acids; propionate, a product of MCP's fermentation and breakdown in the large intestine, directly inhibits both enzymes and also inhibits fatty acid synthesis. The mechanisms affecting enzyme activity involve both feedback regulation at the digestive stage in the intestine and direct effects of breakdown products at the cellular level, making the precise mechanism difficult to determine and warranting further investigation.

(6) Endocrine effects: Polysaccharides have been reported to lower blood glucose by promoting insulin secretion, and insulin in turn increases hepatic cholesterol synthesis as well as the synthesis and secretion of low-density lipoprotein. MCP lowers cholesterol in the body through this pathway. In addition, MCP may lower blood lipids by affecting gastrointestinal hormones such as gastric inhibitory peptide and enteroinsular-like immune responses that produce a low-insulin-like response, exerting its lipid-lowering effect through insulin.

Scavenging of oxygen free radicals MCP lowers blood lipids partly through its antioxidant activity. Various free radicals exist in the body in the form of reactive oxygen species, which can oxidize unsaturated fatty acids in the biological membranes of cells, triggering lipid peroxidation chain reactions involving free radicals. This damages cell membranes and causes disorders of lipid metabolism as well as arteriosclerosis. Polysaccharides can scavenge free radicals in the body, reducing lipid peroxidation of cell membranes and thereby helping to lower blood lipids.

1.2 Mechanism of pectin's blood-sugar-lowering effect

Slowing intestinal absorption of sugars and lipids Numerous studies have shown that pectin from many plants can slow the intestinal absorption of sugars and lipids, thereby helping regulate blood sugar. This may be because pectin's high viscosity increases the viscosity of small intestinal contents, forms a gel layer within the intestine, and increases the thickness of the unstirred mucosal layer, slowing the rate at which glucose moves from the intestinal lumen to the surface of intestinal epithelial cells for absorption, thereby lowering the glucose absorption rate. At the same time, pectin binds with glucose, lowering the effective concentration of glucose in the intestinal fluid. In addition, by encapsulating starch and α-amylase, pectin prevents the amylase from acting effectively, extending the time required for enzymatic breakdown and slowing the rate at which glucose is released into the intestinal fluid.

Regulation of hormone levels Related research indicates that pectin can lower blood glucose levels in both normal and experimentally diabetic rats, an effect closely linked to its promotion of insulin secretion. A possible mechanism is that short-chain fatty acids produced by the fermentation of pectin in the intestine have hormone-regulating effects, promoting the production of glucose-lowering hormones and inhibiting glucose-raising hormones.

Regulation of glucose-metabolizing enzyme activity by polysaccharides Rather than increasing insulin secretion, MCP lowers blood glucose by acting on enzymes involved in glucose metabolism - regulating the activity of glucose-metabolism-related enzymes, promoting glucose utilization, and inhibiting gluconeogenesis - thereby improving disordered glucose metabolism and insulin resistance to achieve a blood-glucose-lowering effect. For example, a pectin-like polysaccharide fraction extracted from the rhizome of Rehmannia glutinosa (Huaiqing dihuang) has been shown to markedly increase the activity of hepatic glucokinase and glucose-6-phosphate dehydrogenase, while lowering the activity of hepatic glucose-6-phosphatase and phosphofructokinase.

1.3 Mechanism of MCP's blood-pressure-lowering effect

Research in recent years has shown that MCP has a good blood-pressure-lowering effect. The mechanisms behind MCP's antihypertensive effect include:

(1) Dietary salt is one of the causes of hypertension. MCP can adsorb sodium-containing compounds in the body and help remove them together through excretion, reducing the absorption rate of dietary salt and thereby helping to lower blood pressure.

(2) MCP can accelerate the conversion and excretion of cholesterol through multiple mechanisms, thereby helping to prevent and address atherosclerosis and hypertension caused by hyperlipidemia.

(3) Hypertension is an important factor that damages arterial endothelial function. Increased vascular wall stress and shear stress, along with elevated levels of vasoactive substances such as noradrenaline and angiotensin II, damage the vascular endothelium early in the course of hypertension. Pectin may lower plasma angiotensin II and endothelin levels, thereby helping to lower blood pressure.

(4) MCP not only directly helps regulate blood pressure through its vasodilatory effect, but is also associated with protecting vascular endothelial cells, inhibiting smooth muscle cell proliferation, regulating platelet aggregation, and influencing myocardial contractile function and cardiomyocyte apoptosis - making it an important factor in cardiovascular disease, including the course of hypertension, where it is considered to play a primarily protective role. Pectin can promote the production of nitric oxide (NO), thereby helping to lower arterial systolic pressure in hypertensive patients. MCP may reduce sympathetic nervous system excitability through central or peripheral pathways, thereby influencing cardiovascular activity.

MCP is recognized by the Food and Agriculture Organization (FAO) and the World Health Organization (WHO) as a safe ingredient with no specified upper limit on daily human intake.

Gold Kropn uses imported lemon peel from Argentina, which undergoes rinsing, dehydration, pesticide residue removal, and heavy metal testing at every stage of processing.

Production takes place in a Class 100,000 GMP-certified clean workshop, applying pharmaceutical-grade standards to food production, with strict controls at every step of the process. The company holds certifications including GMP, ISO 9001, ISO 22000, Kosher, and Halal, and does not use any non-food-grade chemical raw materials (such as colorants, flavorings, or additives) during processing.

MCP is extracted using patented biological enzymatic hydrolysis technology at an internationally leading level.

Numerous renowned scientists, universities, and research institutes around the world have conducted research on MCP.

Within China, research into low molecular weight pectin has been conducted by multiple universities since 2006, including Zhejiang University, Fudan University, Guangzhou Medical University, Tianjin University, and Xinxiang Medical University, among other institutions. Since 2012, Gold Kropn has collaborated with Zhejiang University and Fudan University on a series of functional studies of low molecular weight pectin, including its applications in inhibiting breast cancer, enhancing detoxification sensitization during chemotherapy, and removing heavy metals, and has also worked with the Zhejiang Academy of Medical Sciences on studies of low molecular weight pectin's effect on the "three highs," all of which produced favorable results.