Cinnamaldehyde treatment during adolescence improves white and brown adipose tissue metabolism in a male rat model of early obesity.

Early obesity is a serious health problem and nutritional therapeutic strategies during young age may improve health outcomes throughout life. Cinnamaldehyde, the major component of cinnamon, exhibits several beneficial metabolic effects. Here we tested the impact of cinnamaldehyde treatment during adolescence in a rat model of obesity programmed by early overnutrition, addressing white (WAT) and brown adipose tissue (BAT). After birth, litters were adjusted to 10 pups or 3 pups (small litter) to induce overfeeding and early obesity. On postnatal day 30, half of the small litter pups received cinnamaldehyde (40 mg per kg of body mass per day) for 30 days. The animals were studied at the end of the treatment at 60 days of age and 4 months thereafter (180 days old). The early overfeeding programmed to higher epididymal WAT mass, adipocyte hypertrophy at both ages, and higher BAT mass associated with higher lipid accumulation in the long term. Cinnamaldehyde reduced the adipocyte hypertrophy associated with reduced lipogenesis machinery expression (Srebf1c, Acaca), while it stimulated oxidative ones (Ppargc1a, Fgf21) in WAT, and increased BAT thermogenesis markers (Ppara, Fgf21, Ucp1). In the long term, cinnamaldehyde treatment reprogrammed the metabolism leading to a diminished WAT adipocyte size, accompanied by reduced expression of lipogenesis-related genes (Pparg, Dgat2). In BAT, cinnamaldehyde led to reduced lipogenesis marker expression (Pparg, Lpl) associated with the reduced whitening phenotype, and a robust increase in Fgf21 expression. These results suggest that cinnamaldehyde intake during adolescence has long-lasting benefits in WAT and BAT metabolism, reinforcing its potential as a reprogramming nutraceutical in the treatment of childhood obesity.

Decreased Circulating Levels of APRIL: Questioning Its Role in Diabetes.

Diabetes mellitus is a chronic disease that affects over 382 million people worldwide. Type-1 Diabetes (T1D) is classified as an autoimmune disease that results from pancreatic ß-cell destruction and insulin deficiency. Type-2 Diabetes (T2D) is characterized principally by insulin resistance in target tissues followed by decreased insulin production due to ß-cell failure. It is challenging to identify immunological markers such as inflammatory molecules that are triggered in response to changes during the pathogenesis of diabetes. APRIL is an important member of the TNF family and has been linked to chronic inflammatory processes of various diseases since its discovery in 1998. Therefore, this study aimed to evaluate APRIL serum levels in T1D and T2D. For this, we used the ELISA assay to measure serum APRIL levels of 33 T1D and 30 T2D patients, and non-diabetic subjects as control group. Our data showed a decrease in serum APRIL levels in T1D patients when compared with healthy individuals. The same pattern was observed in the group of T2D patients when compared with the control. The decrease of serum APRIL levels in diabetic patients suggests that this cytokine has a role in T1D and T2D. Diabetes is already considered as an inflammatory condition with different cytokines being implicated in its physiopathology. Our data suggest that APRIL can be considered as a potential modulating cytokine in the inflammatory process of diabetes.