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What is Metabolism?00:52

What is Metabolism?

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Overview
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Carbohydrates consumed through foods are converted into glucose, a crucial energy source for the body. In the prandial state, high blood glucose levels stimulate the secretion of insulin from the pancreas. Insulin inhibits hepatic glucose production and stimulates glucose uptake and metabolism by muscle and adipose tissue. The excess glucose is converted into glycogen and stored in the liver and muscles.
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Glucose Transporters01:27

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Glucose transporters facilitate the transport of glucose across the cell membrane. In addition to glucose, some glucose transporters can also aid the movement of other hexoses such as fructose, mannose, and galactose.
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Glucose Absorption Into the Small Intestine01:26

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Complex carbohydrates consumed cannot be absorbed into the small intestine in their original form. First, they must be hydrolyzed to a monosaccharide form such as glucose or galactose. These monosaccharides are then transported across the intestinal membrane and into the blood via transcellular transport. The intestinal epithelial cells allow the movement of these monosaccharides with a defined 'entry' through membrane transporter proteins present on their apical membrane and...
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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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Carbohydrate Metabolism01:36

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Carbohydrates are polymers composed of molecules containing atoms of carbon, hydrogen and oxygen. One gram of carbohydrate can provide four kilo-calories of energy, which makes it the most efficient instant energy source.
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Related Experiment Video

Updated: Feb 13, 2026

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test OGTT and Insulin Tolerance Test ITT
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Activin in glucose metabolism.

Osamu Hashimoto1, Masayuki Funaba

  • 1Faculty of Veterinary Medicine, Kitasato University, School of Veterinary Medicine, Towada, Aomori, Japan.

Vitamins and Hormones
|March 1, 2011
PubMed
Summary

Activins, part of the TGF-β family, impact glucose metabolism by influencing insulin-producing cells and sensitivity. Modulating activin activity could treat metabolic syndrome by improving insulin responsiveness.

Area of Science:

  • Endocrinology
  • Metabolic Regulation
  • Cell Differentiation

Background:

  • Activins, members of the TGF-β superfamily, are key regulators of cellular processes.
  • They play a critical role in glucose and energy metabolism, influencing insulin sensitivity.
  • Dysregulation of these processes is linked to metabolic disorders like type 2 diabetes.

Purpose of the Study:

  • To investigate the multifaceted roles of activins in regulating glucose metabolism and insulin sensitivity.
  • To explore the tissue-specific effects of activins on insulin-responsive organs and inflammation.
  • To assess the therapeutic potential of targeting activin signaling for metabolic syndrome.

Main Methods:

  • Review of existing literature on activin function in metabolic regulation.

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  • Analysis of activin's impact on pancreatic beta-cell differentiation and insulin secretion.
  • Examination of activin's effects on insulin sensitivity in liver, muscle, and adipose tissue.
  • Investigation of activin-mediated macrophage polarization and its anti-inflammatory effects.
  • Main Results:

    • Activins promote pancreatic beta-cell differentiation and insulin secretion.
    • Conversely, activins negatively regulate organogenesis in liver, muscle, and adipose tissue, impairing insulin sensitivity.
    • Activins induce a shift in macrophages from M1 to M2 phenotypes, reducing inflammation.
    • Adipose inflammation is a key factor in insulin resistance and type 2 diabetes.

    Conclusions:

    • Activin's influence on insulin sensitivity is tissue-dependent, necessitating localized regulation.
    • The anti-inflammatory properties of activins suggest a role in improving insulin resistance.
    • Activins or their inhibitors show promise as therapeutic agents for metabolic syndrome.