TITLE:
The Effect of Tuberculosis Infection on Pancreatic Beta-Cell Function in Patients with Type 2 Diabetes Mellitus
AUTHORS:
Mengdan Kong, Ailin Zhong, Shilin Qu, Junli Xue
KEYWORDS:
Tuberculosis Infection, Type 2 Diabetes Mellitus, Pancreatic β-Cell Function, Insulin Resistance
JOURNAL NAME:
Advances in Bioscience and Biotechnology,
Vol.15 No.2,
February
9,
2024
ABSTRACT: Objective: The aim of this study is to investigate how individuals with type 2
diabetes mellitus’ pancreatic β-cell
function index and insulin resistance index are affected by tuberculosis
infection. Methods: The study group consisted of 89 patients with type 2
diabetes mellitus and tuberculosis infection who
were admitted to Jingzhou Chest Hospital between March 2019 and March
2021. Gender and duration of diabetes were matching conditions. The control
group was made up of 89 patients with type 2 diabetes who were admitted to
Jingzhou Central Hospital’s endocrinology department during the same period. The two patient groups provided general information
such as gender, age, length of diabetes, and blood biochemical indexes such as glycosylated
hemoglobin (HbA1c), fasting glucose (FPG), and fasting C-peptide (FC-P). The
HOMA calculator was used to calculate the HOMA-β and the HOMA-IR, and intergroup comparisons and correlation
analyses were carried out. Results: Regarding gender, age, disease
duration, FC-P, and HbA1c, the differences between the two groups were not
statistically significant (P > 0.05).
However, BMI, FPG, HOMA-β, and
HOMA-IR showed statistically significant differences (P study group’s HOMA-β was lower and
its HOMA-IR was greater. According to Spearman’s correlation
analysis, HOMA-β had a negative
association (P th
FPG, HbA1c, and the length of the disease, and a positive correlation with BMI
and FC-P. A positive correlation was found between HOMA-IR and
BMI, FPG, and FC-P (P 0.05) and HbA1c. Conclusions: In type 2 diabetes
mellitus combined with tuberculosis infection, the patients had higher FPG
levels and lower FC-P levels, the secretory function of pancreatic β-cells was more severely impaired, and
insulin resistance was more obvious.