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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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Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
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MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
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Glucose Homeostasis: Regulation of Blood Glucose

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Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library
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Published on: April 6, 2012

MicroRNA-29a-c decrease fasting blood glucose levels by negatively regulating hepatic gluconeogenesis.

Jichao Liang1, Changzheng Liu, Aijun Qiao

  • 1Hubei Province Key Laboratory of Biotechnology of Chinese Traditional Medicine, Hubei University, Wuhan 430062, China.

Journal of Hepatology
|November 1, 2012
PubMed
Summary
This summary is machine-generated.

MicroRNA-29 (miR-29a-c) upregulation in diabetic mouse livers improves glucose tolerance. These microRNAs reduce hepatic glucose production by targeting PGC-1α and G6Pase, forming a feedback loop.

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Area of Science:

  • Molecular biology
  • Metabolic diseases
  • Genetics

Background:

  • MicroRNA-29 (miR-29) family members (miR-29a-c) are upregulated in the livers of diabetic animal models.
  • The functional impact of this upregulation on hepatic glucose metabolism remains unexplored.

Purpose of the Study:

  • To investigate the role of miR-29a-c in regulating hepatic glucose production.
  • To evaluate the effect of miR-29a-c on blood glucose levels and glucose tolerance in vivo and in vitro.

Main Methods:

  • Adenovirus-mediated overexpression and loss-of-function studies of miR-29a-c in mouse models (db/m, db/db, DIO) and primary hepatocytes.
  • Assessment of blood glucose levels, glucose tolerance, and pyruvate tolerance tests.
  • Identification of direct miR-29a-c targets involved in glucose metabolism.

Main Results:

  • Overexpression of miR-29a-c in diabetic and obese mice decreased fasting blood glucose and improved glucose tolerance.
  • miR-29a-c reduced hepatic glucose production by decreasing protein levels of PGC-1α and G6Pase.
  • Loss of miR-29a-c function increased PGC-1α and G6Pase, leading to higher glucose production.
  • Enforced PGC-1α expression increased miR-29a-c, indicating a negative feedback loop.

Conclusions:

  • miR-29a-c plays a crucial role in regulating hepatic glucose production.
  • miR-29a-c can improve glucose tolerance in mice, suggesting therapeutic potential for diabetes.