[Latin Name] Amorphophallus konjac

[Plant Source] from China

[Specifications] Glucomannan85%-90%

[Appearance] White or cream-color powder

Plant Part Used:Root

[Particle size] 120 Mesh

[Loss on drying] ≤10.0%

[Heavy Metal] ≤10PPM

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

[Shelf life] 24 Months

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

[Net weight] 25kgs/drum

[Introduction]

Konjac is a plant that is found in China, Japan and Indonesia. The plant is part of the genus Amorphophallus. Typically, it thrives in the warmer regions of Asia.

The extract of the Konjac root is referred to as Glucomannan. Glucomannan is a fiber-like substance traditionally used in food recipes, but now it is utilized as an alternative means of weight loss. Along with this benefit, konjac extract contains other benefits for the rest of the body as well.

The main material of the natural konjac gum is fresh konjac, which grow in virgin forest in Hubei area. We use advanced method to distill the KGM, aminophenol, Ca, Fe, Se which are good for health. Konjac is known as“ the seventh nutriment for human”.

Konjac Gum with its special water holiding capacity, stability, emulsibility, thickening property,suspension property and gel propery can especially adopted in food industry.

[Main Function]

1.It could reduce postprandial glycemia, blood cholesterol and blood pressure.

2.It could control appetite and reduce body weight.

3.It could increase insulin sensitivity.
4.It could control insulin resistant syndrome and diabetesII development.
5.It could reduce heart disease.

[Application]

1) Gelatinizer(jelly, pudding, Cheese, soft candy, jam );

2) Stabilizer(meat, beer);

3) Film Former(capsule, preservative)

4) Water-keeping agent( Baked Foodstuff );

5) Thickener (Konjac Noodles, Konjac Stick, Konjac Slice, Konjac Imitating Food stuff);

6) Adherence agent( Surimi );

7) Foam Stabilizer (ice cream, cream, beer)

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“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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