Elevated IMTGs in young streptozotocin‐induced diabetic rats

Intramuscular triglycerides (IMTGs) are lipid stores created from non‐esterified fatty acids found in skeletal muscle tissue that are an important energy source for exercise. High IMTGs levels have been linked to insulin resistance, type 2 diabetes and are also elevated in humans with type 1 diabetes mellitus (TIDM) and in rodents several weeks following streptozotocin (STZ) treatment. It is unclear, however, whether the increase in IMTGs is a result of insulin resistance, reduced rates of IMTG oxidation or from hypoinsulinemia and the subsequent elevation in circulating free fatty acids. To help address this, we treated 3 male Sprague‐Dawley rats with STZ and harvested soleus muscle 48 hours later. IMTGs were quantified by Oil‐Red‐O staining in dehydrated soleus muscle sections. Compared with age‐matched controls, STZ rats had higher blood glucose (31.1 ± 3.1 vs. 6.6 ± 0.2 mmol/L, p<0.01), reduced body mass (181.0 ± 6.4 vs. 199.3 ± 4.7 g, p<0.02), and higher plasma corticosterone levels (118.0 ± 53.8 vs. 16.3 ± 1.5 ng/ml, p<0.05). IMTG levels, expressed as percent of fibre area, were approximately 18‐fold higher in the STZ group (1.8 ± 2.3 vs. 33.0 ± 12.9 %, p<0.01). Preliminary data suggests that insulin restoration normalizes IMTG levels (STZ + insulin = 3.6 ± 4.8 %; n=2). These data support our belief that the increase in FFA levels with hypoinsulinemia promptly and dramatically increases IMTG levels and that insulin restoration restores this defect in T1DM.