[Latin Name] Curcuma longa L.

[Plant Source] Root From India

[Specification] Curcuminoids 95% HPLC

[Appearance] Yellow powder

Plant Part Used: Root

[Particle size]80Mesh

[Loss on drying] ≤5.0%

[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

[What is Curcuma Longa?]

Turmeric is an herbaceous plant known scientifically as Curcuma longa. It belongs to the Zingiberaceae family, which includes ginger. Tumeric has rhizomes rather than true roots, which are the primary source of commercial value for this plant. Tumeric originates from southwest India, where it has been a stable of Siddha medicine for thousands of years. It is also a common spice in Indian cuisine and is often used as flavoring for Asian mustards.

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Furthermore, we have found a broad range of natural substances experimentally confirmed to stimulate beta cell regeneration, 10 of which are listed below:

Arginine: a 2007 study found that the amino acid L-arginine is capable of stimulating the genesis of beta cells in an animal model of alloxan-induced diabetes.[2]
Avocado: A 2007 study found that avocado seed extract reduced blood sugar in diabetic rats. Researchers observed a restorative and protective effect on pancreatic islet cells in the treated group.[3]
Berberine: A 2009 study found that this plant compound, commonly found in herbs such as barberry and goldenseal, induces beta cell regeneration in diabetic rats, which lends explanation for why it has been used for 1400 years in China to treat diabetes.[4]
Chard: A 2000 study found that chard extract given to diabetic rats stimulates the recovery of injured beta cells.[5]
Corn Silk: A 2009 study found that corn silk reduces blood sugar and stimulates beta cell regeneration in type 1 diabetic rats.[6]
Curcumin (from Turmeric): A 2010 study found that curcumin stimulates beta cell regeneration in type 1 diabetic rats.[7] Additionally, a 2008 study found that curcumin preserves pancreatic islet cell survival and transplantation efficiency.[8]
Genistein (from soy, red clover): A 2010 study found that genistein induces pancreatic beta-cell proliferation through activation of multiple signaling pathways and prevents insulin-deficient diabetes in mice.[9]
Honey: A 2010 human study found that long-term consumption of honey might have positive effects on the metabolic derangements of type 1 diabetes, including possible beta cell regeneration as indicating by increases in fasting C-peptide levels.[10]
Nigella Sativa (black seed): A 2003 animal study found that black seed consumption lead to partial regeneration/proliferation of the beta-cells.[11] A 2010 human study also found that the consumption of one gram of black seed a day for up to 12 weeks had a broad range of beneficial effects in diabetics, including increasing beta cell function.[12]
Stevia: A 2011 human study found that stevia has anti-diabetic properties, including revitalizing damaged beta cells, and compares favorably with the drug glibenclamide but without the adverse effects.[13]

“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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