Transforming growth factor β<sub>1</sub> at clinical onset of Type 1 diabetes mellitus. A pilot study

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<jats:title>Abstract</jats:title><jats:p><jats:bold>Aims </jats:bold> The aims of the study were to determine whether transforming growth factor β<jats:sub>1</jats:sub> TGF‐β<jats:sub>1</jats:sub> levels are raised at diagnosis of Type 1 diabetes mellitus and are related to blood glucose.</jats:p><jats:p><jats:bold>Subjects and methods </jats:bold> Fourteen patients (mean age 24.3 ± 4.9 years) admitted to hospital for onset of Type 1 diabetes were studied. On the first day of hospitalization, before insulin therapy, and at 1, 4 and 16 weeks, fasting blood glucose, HbA<jats:sub>1c</jats:sub>, lipid profile and TGF‐β<jats:sub>1</jats:sub> levels and TGF‐β<jats:sub>1</jats:sub> levels in 24‐h urine were determined. The control group included 14 non‐diabetic subjects with similar characteristics to those of the diabetic group.</jats:p><jats:p><jats:bold>Results </jats:bold> Plasma and urinary TGF‐β<jats:sub>1</jats:sub> levels were significantly lower in controls (4.7 (1.6–6.8) ng/ml <jats:italic>P</jats:italic> < 0.001; 5.7 (1.5–8.5) ng/mg urinary creatinine, <jats:italic>P</jats:italic> < 0.01) than in patients with Type 1 diabetes mellitus [10.5 (1.8–24.9) ng/ml; 10.1 (4.2–29.8) ng/mg urinary creatinine]. On study completion, HbA<jats:sub>1c</jats:sub> fell from 11.6 ± 2.0 to 5.4 ± 0.6% (<jats:italic>P</jats:italic> < 0.001). Improved metabolic control was not associated with changes in plasma (9.4 (2.6–19.5)/5.9 (1.6–21.5)/7.0 (2.3–30.2)/10.5 (1.8–24.9) ng/ml at baseline, 1, 4 and 16 weeks, respectively) or urinary (12.0 (4.7–29.5)/10.9 (1.5–20.5)/8.7 (4.3–16.9)/10.1 (4.2–29.8) ng/mg urinary creatinine) TGF‐β<jats:sub>1</jats:sub> levels. A statistically significant correlation was observed between plasma TGF‐β<jats:sub>1</jats:sub> and insulin dosage (U/kg/day) (<jats:italic>r</jats:italic> = 0.52, <jats:italic>P</jats:italic> = 0.037).</jats:p><jats:p><jats:bold>Conclusions </jats:bold> The increased TGF‐β<jats:sub>1</jats:sub> production observed herein was not modulated by glycaemic reduction and could be a response to immuno‐inflammatory activation present at the onset of Type 1 diabetes.</jats:p>

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