Insulin resistance in nonobese type 2 diabetic Goto Kakizaki rats is associated with a proinflammatory T lymphocyte profile.

Goto-Kakizaki (GK) rats develop a well-defined insulin resistance (IR) and type 2 diabetes mellitus (T2DM) without presenting obesity. The lymphocyte profile in nonobese diabetic conditions is not yet characterized. Therefore, GK rats were chosen to explore T lymphocyte (TL) dynamics at various stages (21, 60, and 120 days) compared to Wistar rats. GK rats exhibit progressive disruption of glucose regulation, with early glucose intolerance at 21 days and reduced insulin sensitivity at 60 days, confirming IR. Glucose transporter 1 (GLUT1) expression was consistently elevated in GK rats, suggesting heightened TL activation. T-regulatory lymphocyte markers diminished at 21 days. However, GK rats showed increased Th1 markers and reduced Gata-3 expression (crucial for Th2 cell differentiation) at 120 days. These findings underscore an early breakdown of anti-inflammatory mechanisms in GK rats, indicating a proinflammatory TL profile that may worsen chronic inflammation in T2DM.

Glutamine supplementation versus functional overload in extensor digitorum longus muscle hypertrophy

Background Glutamine levels directly associate with total protein content in cultured skeletal muscle cells, whereas glutamine supplementation enhances skeletal muscle mass in catabolic experimental conditions. Methods We compared the effect of glutamine administration on Extensor Digitorum Longus muscle (EDL) weight, fiber cross-sectional area (CSA), contractile activity, and protein metabolism signaling with a functional overload-induced skeletal muscle hypertrophy protocol. Results Glutamine supplementation raised the predominance of EDL muscle fibers with CSA between 1001 and 2000 μm2 (49.7 %), the p-4E-BP1/total 4E-BP1 ratio, and the effect of overload on resistance to fatigue. The proportion of the EDL muscle fiber CSA distribution for the combination of both treatments was similar to that induced by overload or glutamine separately; 54.3 % muscle fibers with CSA between 1001 and 2000 μm². Glutamine supplementation did not markedly affect the changes induced by overload on protein synthesis signaling pathways, except for a further increase of the p-4E-BP1/total 4E-BP1 ratio. Conclusions The effect of glutamine on EDL muscle fiber CSA distribution and protein synthesis signaling mimicked the response to overload. The association of glutamine and overload induced EDL muscle hypertrophy further increased the resistance to fatigue.