[Latin Name] Camellia sinensis

[Plant Source] China

[Specifications]

Total tea polyphenols 40%-98%

Total catechins 20%-90%

EGCG 8%-60%

[Appearance] Yellow brown powder

[Plant Part Used] Green tea leaf

[Particle size] 80 Mesh

[Loss on drying] ≤5.0%

[Heavy Metal] ≤10PPM

[Storage] Store in cool & dry area, keep away from the direct light and heat.

[Package] Packed in paper-drums and two plastic-bags inside.

[What is green tea extract]

Green tea is the second largest beverage demanded by consumers worldwide. Used in China and India for its medicinal effects. There are several compounds extracted from green tea including catechins which contain an enormous amount of hydroxyphenols that are easily oxidized, congregated and contracted, which explains its good anti-oxidation effect. Its anti-oxidation effect is 25-100 times as strong as those of vitamin C and E.

It is widely used in medicines, agriculture, and chemical and food industries. This extract prevents cardio-vascular disease, lowers the risk of cancer, and decreases blood sugar and blood pressure, as well as viruses. In the food industry, the anti-oxidation agent used for preserving food and cooking oils.

[Function]

1. Green tea extract can reduce blood pressure, blood sugar, blood lipids.

2. Green tea extract has the function of removing radicals and anti-aging.

3. Green tea extract can enhance the immune function and prevention of colds.

4. Green tea extract will anti-radiation,anti-cancer, inhibiting the increasing of cancer cell.

5. Green tea extract used to anti-bacterium, with the function of sterilization and deodorization.

[Application]

1.Applied in cosmetics field, Green tea extract owns the effect of anti-wrinkle and anti-Aging.

2.Applied in food field, Green tea extract is used as natural antioxidant, antistaling agent, and anti-fading agents.

3.Applied in pharmaceutical field, Green tea extract is used to prevent and cure cardiovascular disease, diabetes.

This tutorial discusses polysaccharides, specifically the difference between amylose, amlyopectin, glcogen, and cellulose.

“Equine Polysaccharide Storage Myopathy” is an inheritable glycogen storage disease of horses that causes exertional rhabdomyolysis. It is most commonly associated with heavy horse breeds and the American Quarter Horse. While incurable, PSSM can be managed with appropriate diet and exercise. There are currently 2 subtypes, known as Type 1 PSSM and Type 2 PSSM.

Glycogen is a molecular polymer of glucose used to store energy, and is important for maintaining glucose hemostasis in the blood, as well as for providing energy for skeletal muscle and cardiac muscle contraction. Molecules of glucose are linked into linear chains by α-1,4-glycosidic bonds. Additionally, branches of glucose are formed off of the chain by α-1,6-glycosidic bonds. 2 molecules of glucose are joined into an α-1,4-glycosidic bonds by an enzyme known as glycogen synthase. This bond may be broken by amylase when the body wishes to break down glycogen into glucose for energy. Glycogen branching enzyme is responsible for the required α-1,6-glycosidic bonds needed to start a branch off of these linear chains.

Any disruption to this system results in a glycogen storage disease. There are currently 3 subcategories of glycogen storage diseases in horses: Type 1 Polysaccharide Storage Myopathy, Glycogen Branching Enzyme Deficiency , and Type 2 Polysaccharide Storage Myopathy.

Type 1 PSSM is caused by an autosomal dominant genetic mutation known as GSY1. This mutation causes an up-regulation of glycogen synthase, and high levels of glycogen synthase relative to glycogen branching enzyme . This altered ratio of glycogen synthase to GBE results in glycogen molecules with long chains and few branches, making these molecules somewhat amylase resistant. The GSY1 mutation is associated with altered glucose metabolism , as well as accumulation of high levels of glycogen and abnormal polysaccharide in the muscles of the horse. Additionally, some horses have been shown to have insulin sensitivity, which improves glucose uptake by muscle cells and contributes to excessive glycogen storage that is already elevated secondary to the GSY1 mutation.

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