Pancreatic Fat is not significantly correlated with β-cell Dysfunction in Patients with new-onset Type 2 Diabetes Mellitus using quantitative Computed Tomography.

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  • Additional Information
    • Source:
      Publisher: Ivyspring International Publisher Country of Publication: Australia NLM ID: 101213954 Publication Model: eCollection Cited Medium: Internet ISSN: 1449-1907 (Electronic) Linking ISSN: 14491907 NLM ISO Abbreviation: Int J Med Sci Subsets: MEDLINE
    • Publication Information:
      Original Publication: [Australia] : Ivyspring International Publisher, c2004-
    • Subject Terms:
      Adipose Tissue/*diagnostic imaging ; Diabetes Mellitus, Type 2/*diagnosis ; Insulin-Secreting Cells/*pathology ; Pancreas/*diagnostic imaging; Adipose Tissue/pathology ; Adult ; Blood Glucose/genetics ; Body Mass Index ; Diabetes Mellitus, Type 2/diagnostic imaging ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/pathology ; Female ; Glucose Tolerance Test ; Humans ; Insulin/metabolism ; Insulin Resistance/genetics ; Insulin-Secreting Cells/metabolism ; Intra-Abdominal Fat/diagnostic imaging ; Intra-Abdominal Fat/metabolism ; Liver/metabolism ; Liver/pathology ; Male ; Middle Aged ; Pancreas/pathology ; Tomography, Emission-Computed
    • Abstract:
      Objective: Type 2 diabetes mellitus (T2DM) is a chronic condition resulting from insulin resistance and insufficient β-cell secretion, leading to improper glycaemic regulation. Previous studies have found that excessive fat deposits in organs such as the liver and muscle can cause insulin resistance through lipotoxicity that affects β-cell function. The relationships between fat deposits in pancreatic tissue, the function of β-cells, the method of visceral fat evaluation and T2DM have been sought by researchers. This study aims to elucidate the role of pancreatic fat deposits in the development of T2DM using quantitative computed tomography (QCT), especially their effects on islet β-cell function. Methods: We examined 106 subjects at the onset of T2DM who had undergone abdominal QCT. Estimated pancreatic fat and liver fat were quantified using QCT and calculated. We analysed the correlations with Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) scores and other oral glucose tolerance test-derived parameters that reflect islet function. Furthermore, correlations of estimated pancreatic fat and liver fat with the area under the curve for insulin (AUC INS ) and HOMA-IR were assessed with partial correlation analysis and demonstrated by scatter plots. Results: Associations were found between estimated liver fat and HOMA-IR, AUC INS , the modified β-cell function index (MBCI) and Homeostatic Model Assessment β (HOMA-β). However, no significant differences existed between estimated pancreas fat and those parameters. Similarly, after adjustment for sex, age and body mass index, only estimated liver fat was correlated with HOMA-IR and AUC INS . Conclusions: This study suggests no significant correlation between pancreatic fat deposition and β-cell dysfunction in the early stages of T2DM using QCT as a screening tool. The deposits of fat in the pancreas and the resulting lipotoxicity may play an important role in the late stage of islet cell function dysfunction as the course of T2DM progresses.
      Competing Interests: Competing Interests: The authors have declared that no competing interest exists.
      (© The author(s).)
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    • Contributed Indexing:
      Keywords: Insulin resistance; Onset type 2 diabetes mellitus; Pancreatic fat; Quantitative computed tomography; β-cell function
    • Accession Number:
      0 (Blood Glucose)
      0 (Insulin)
    • Publication Date:
      Date Created: 20200728 Date Completed: 20210601 Latest Revision: 20210601
    • Publication Date:
      20240628
    • Accession Number:
      PMC7378671
    • Accession Number:
      10.7150/ijms.46395
    • Accession Number:
      32714070