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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

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A Method for Mouse Pancreatic Islet Isolation and Intracellular cAMP Determination
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Structure-functional changes in eNAMPT at high concentrations mediate mouse and human beta cell dysfunction in type 2

Sophie R Sayers1, Rebecca L Beavil2, Nicholas H F Fine3,4,5

  • 1Diabetes Research Group, Department of Diabetes, School of Life Course Sciences, King's College London, Hodgkin Building, Guy's Campus, London, SE1 1UL, UK.

Diabetologia
|November 17, 2019
PubMed
Summary
This summary is machine-generated.

Extracellular nicotinamide phosphoribosyltransferase (eNAMPT) has dual effects on beta cells. At low levels, dimer eNAMPT supports function, but high levels, as seen in type 2 diabetes, lead to monomeric eNAMPT causing dysfunction and apoptosis.

Keywords:
Beta cellExtracellularnicotinamide phosphoribosyltransferaseInflammationInsulin secretionNADType 2 diabeteseNAMPT

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Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Molecular Biology

Background:

  • Progressive decline in functional beta cell mass is central to type 2 diabetes development.
  • Elevated extracellular nicotinamide phosphoribosyltransferase (eNAMPT) is linked to beta cell failure, yet its precise effects are unclear.
  • eNAMPT exists in monomeric and dimeric forms, with dimerisation crucial for NAD-biosynthesis, while monomers may have distinct NAD-independent roles.

Purpose of the Study:

  • To fully characterize the structure-functional effects of eNAMPT on pancreatic beta cell functional mass.
  • To elucidate the role of eNAMPT in beta cell failure associated with type 2 diabetes.

Main Methods:

  • Utilized CD-1 mice and human islets, generating recombinant monomeric and wild-type eNAMPT.
  • Assessed beta cell function via insulin secretion and calcium microfluorimetry.
  • Analyzed NAD-biosynthetic capacity, islet cell number, apoptosis, and inflammatory markers.

Main Results:

  • eNAMPT exhibits bimodal, concentration- and structure-dependent effects on beta cell mass.
  • Low physiological eNAMPT concentrations (dimeric form) enhance beta cell function via NAD-dependent mechanisms.
  • High eNAMPT concentrations (~5 ng/ml, monomeric form) induce beta cell dysfunction, reduced identity, increased apoptosis, and inflammation via NAD-independent pathways.

Conclusions:

  • A novel mechanism for type 2 diabetes beta cell dysfunction involving eNAMPT structure-function changes is identified.
  • Dimeric eNAMPT maintains beta cell function at low levels, while elevated monomeric eNAMPT in type 2 diabetes induces a diabetic phenotype.
  • Targeting monomeric eNAMPT presents a potential therapeutic strategy for type 2 diabetes.