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Updated: Aug 10, 2026

Sample Preparation of Mycobacterium tuberculosis Extracts for Nuclear Magnetic Resonance Metabolomic Studies
07:56

Sample Preparation of Mycobacterium tuberculosis Extracts for Nuclear Magnetic Resonance Metabolomic Studies

Published on: September 3, 2012

[Changes in carbohydrate metabolism in patients with tuberculosis]

M A Karachunskiĭ, M I Balabolkin, N R Beglarian

    Vestnik Rossiiskoi Akademii Meditsinskikh Nauk
    |January 1, 1995
    PubMed

    Insights

    Pulmonary tuberculosis patients show enhanced insulin secretion but also signs of relative insulin deficiency, increasing diabetes risk. This suggests a complex interplay between tuberculosis and pancreatic function.

    Area of Science:

    • Endocrinology
    • Pulmonology
    • Metabolic Research

    Background:

    • Pulmonary tuberculosis (PTB) is a significant global health challenge.
    • The relationship between PTB and metabolic dysfunction, particularly diabetes mellitus, is increasingly recognized.
    • Understanding the pancreatic incretory function in PTB is crucial for managing comorbidities.

    Purpose of the Study:

    • To investigate the function of the pancreatic incretory apparatus in patients with primary active pulmonary tuberculosis.
    • To analyze blood glucose, immunoreactive insulin, and C-peptide levels in response to glucagon stimulation.
    • To assess the impact of prednisolone therapy on pancreatic function in these patients.

    Main Methods:

    • Studied 51 patients with primary active pulmonary tuberculosis.
    • Analyzed blood levels of immunoreactive insulin, C-peptide, and glucose.
    • Performed glucagon stimulation tests before and after therapy.

    Main Results:

    • Observed pronounced enhanced insulin secretion.
    • Identified signs of relative insulin deficiency, including persistent hyperglycemia and delayed insulin/C-peptide peaks.
    • Prednisolone therapy temporarily worsened relative insulin deficiency.

    Conclusions:

    • Patients with PTB exhibit a complex pancreatic response with both hypersecretion and relative insulin deficiency.
    • Decreased functional reserves of the pancreatic insular apparatus may contribute to severe diabetes development in PTB.
    • Disease duration appears to influence the risk of developing diabetes mellitus in PTB patients.

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