Fatty liver with abnormal glucose metabolism in relation to clinical research. Table 2 results. Table 2 shows the laboratory determination results and comparison of relevant indices (X ± S) for the fatty liver group and non-fatty liver group. Note: Comparison between the two groups: *P < 0.05, **P < 0.01, ***P < 0.001.
In a study involving 78 subjects with fatty liver but without abnormal glucose metabolism, they were divided into a treatment group (taking fenofibrate) and a non-treatment group, with three years of follow-up. The results are as follows: In the treatment group, 2 cases developed impaired glucose tolerance (IGT), with an incidence rate of 4.7%. In the non-treatment group, 8 cases developed IGT, with an incidence of 22.2%, and 6 cases progressed to type 2 diabetes, with an incidence rate of 16.6%.
The laboratory index results for the two groups are shown in Table 3. Table 3 presents the observed determination results and comparisons of relevant indices before and after treatment for treated and untreated fatty liver patients (X+S). Note: Group comparison before and after treatment: *P < 0.05, **P < 0.01; comparison between the two groups: *P < 0.05, **P < 0.01, ***P < 0.001.
Discussion: High triglycerides (TG) hyperinsulinemia induces insulin resistance (IR), reducing peripheral tissue sensitivity to insulin, leading to abnormal glucose metabolism in L3. High TG levels increase intrahepatic fat accumulation, causing fatty liver. Abnormal glucose metabolism is common in many patients and often occurs in nonalcoholic steatohepatitis (NASH). A study followed up on 88 nondiabetic patients with nonalcoholic fatty liver for 5 years and found that 49 cases developed diabetes, with an incidence rate exceeding 50%.
Among 126 patients diagnosed with fatty liver by B-mode ultrasonography, 108 cases of fatty liver were selected for comparison. The results showed that the incidence of abnormal glucose tolerance (IGT) in the fatty liver group was 23.8%, and the incidence of type 2 diabetes was 14.2%. In the non-fatty liver group, the IGT incidence rate was 8.3%, and the incidence of type 2 diabetes was 3.7%. Blood glucose, insulin levels, and insulin resistance index were significantly higher in the fatty liver group than in the non-fatty liver group. These results indicate a close relationship between fatty liver and abnormal glucose metabolism, confirming that fatty liver is an integral part of insulin resistance syndrome [5L].
Given the relationship between fatty liver and abnormal glucose metabolism, treatment can produce effects on glucose metabolism. This report addresses relevant aspects. In this paper, 78 subjects with abnormal glucose metabolism in the fatty liver group were divided into a treatment group and a non-treatment group. After three years of follow-up, only 2 cases of IGT were found in the treatment group, compared to 8 cases of IGT and 6 cases progressing to type 2 diabetes in the non-treatment group.
Before and after treatment, there were no significant changes in blood glucose levels in the treatment group, but insulin content and the insulin resistance index decreased significantly after treatment compared to before treatment. In contrast, in the non-treatment group, blood sugar, insulin content, and the insulin resistance index increased after three years compared to three years ago.
The results suggest that intervention in fatty liver can reduce insulin resistance and improve glucose metabolism. The impact of abnormal glucose metabolism on liver metabolism is the most direct factor in the formation of fatty liver, although it remains inconclusive whether nondiabetic nonalcoholic fatty liver is caused by abnormal glucose metabolism, which should be given attention. We believe that effective treatment for patients with fatty liver may delay or prevent the occurrence of abnormal glucose metabolism, which has certain clinical significance in expanding the scope of prevention and treatment of abnormal glucose metabolism.