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Oral Hypoglycemic Agents: α-Glucosidase Inhibitors01:19

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α-glucosidase inhibitors, including acarbose (Precose), miglitol (Glyset), and voglibose (Voglib) (primarily available in Asia), are drugs that control blood sugar levels by delaying the digestion of starch and disaccharides. They achieve this by inhibiting α-glucosidase enzymes in the intestine, which slow the absorption of carbohydrates in the intestine, which in turn leads to a prolonged release of the glucoregulatory hormone GLP-1 from intestinal L-cells.
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Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a...
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Diabetic Neuropathy01:22

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DefinitionDiabetic neuropathy is nerve damage caused by long-standing diabetes mellitus. It results directly from prolonged high blood sugar levels.PathophysiologyThe pathophysiology of diabetic neuropathy involves both metabolic and vascular disturbances triggered by chronic hyperglycemia.Metabolic injury: Elevated glucose levels activate the polyol pathway within nerve cells, leading to the accumulation of sorbitol and fructose. This increases oxidative stress, disrupts normal nerve...
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Glucagon-like Receptor Agonists01:24

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Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
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Oral Hypoglycemic Agents: Biguanides and Glitazones01:26

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Biguanides, particularly metformin (Glucophage), are insulin sensitizers that enhance glucose uptake, thereby reducing insulin resistance. Unlike sulfonylureas, metformin doesn't prompt insulin secretion, which helps to curb hypoglycemia risk. Metformin is beneficial in treating conditions like polycystic ovary syndrome due to its insulin-resistance reduction capability. The drug's primary action involves curtailing hepatic gluconeogenesis, a significant contributor to high blood...
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Oral Hypoglycemic Agents: Glinides01:06

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Repaglinide (Prandin) and Nateglinide (Starlix), known as glinides, are oral insulin secretagogues that stimulate insulin release from pancreatic β cells by closing the ATP-sensitive potassium channels (KATP channel). Repaglinide controls insulin release from pancreatic β cells by managing potassium efflux. It shares two binding sites with sulfonylureas and also has a unique site, indicating overlapping mechanisms of action. With a rapid onset and a 4-7 hour duration, it effectively...
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Comparative Study on the Polysaccharide Contents and Antioxidant Activities of Hippophae rhamnoides subsp. sinensis and Hippophae gyantsensis
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Anti-diabetic effect mediated by Ramulus mori polysaccharides.

Lingyuan Xu1, Fenglian Yang2, Junli Wang3

  • 1Department of Pharmacy, Affiliated Hospital of YouJiang Medical University for Nationalities, Baise, Guangxi 533000, PR China.

Carbohydrate Polymers
|December 16, 2014
PubMed
Summary

Ramulus mori polysaccharides (RMP) effectively treat diabetes by lowering blood sugar and increasing insulin in mice. RMP protects pancreatic cells from damage and reduces apoptosis, improving metabolic function.

Keywords:
ApoptosisHyperglycemiaMetabolismRamulus mori polysaccharides

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Area of Science:

  • Metabolic disease research
  • Endocrinology
  • Pharmacology

Background:

  • Diabetes mellitus is a complex metabolic disorder.
  • Pancreatic beta-cell apoptosis contributes to diabetes pathogenesis.
  • Streptozotocin (STZ) is commonly used to induce experimental diabetes.

Purpose of the Study:

  • To evaluate the therapeutic potential of Ramulus mori polysaccharides (RMP) in a mouse model of diabetes.
  • To investigate the effects of RMP on pancreatic cell apoptosis and metabolic function.

Main Methods:

  • Induction of diabetes in mice using streptozotocin (STZ).
  • Administration of RMP to diabetic mice.
  • Assessment of glycemic control (blood glucose, HbA1c, insulin levels).
  • Histopathological examination of pancreatic tissue.
  • Analysis of apoptosis-related protein expression (Bcl-2, Bax) and signaling pathways (JNK, p38, caspase-3).

Main Results:

  • RMP treatment significantly lowered hyperglycemia and increased insulin levels in STZ-induced diabetic mice.
  • Histological analysis showed RMP reduced STZ-induced pancreatic cell damage.
  • RMP decreased HbA1c levels.
  • RMP modulated Bcl-2 and Bax protein expression, indicating an anti-apoptotic effect.
  • RMP downregulated the expression of p-JNK, p-p38, and cleaved-caspase-3 in pancreatic tissue.

Conclusions:

  • RMP demonstrates significant hypoglycemic effects in experimental diabetes.
  • RMP protects pancreatic tissue from STZ-induced apoptosis, likely through the regulation of the JNK/p38 signaling pathway.
  • RMP holds promise as a therapeutic agent for ameliorating pancreatic metabolic dysfunction in diabetes.