Publications by authors named "Ludovic Breasson"
Article Synopsis
- PI3Kγ, a member of the phosphatidylinositides-3 kinases family, plays a complex role in liver cancer (HCC) development, particularly in the context of obesity and insulin resistance.
- In studies with mice, removing PI3Kγ led to reduced tumor growth in cases of HCC associated with obesity, despite no apparent change in lean mice.
- The findings suggest that targeting PI3Kγ could offer a new strategy for treating or preventing obesity-related HCC by improving metabolic conditions and reducing inflammation.
The cJun N-terminal Kinases (JNK) emerged as a major link between obesity and insulin resistance, but their role in the loss of pancreatic β-cell mass and function driving the progression from insulin resistance to type-2 diabetes and in the complications of diabetes was not investigated to the same extent. Furthermore, it was shown that pan-JNK inhibition exacerbates kidney damage in the db/db model of obesity-driven diabetes. Here we investigate the role of JNK1 in the db/db model of obesity-driven type-2 diabetes.
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- PI3Kγ is a potential treatment target for obesity and insulin resistance, but its role in normal insulin secretion from pancreatic β cells raises concerns about its inhibition.
- Research on diabetic mice lacking PI3Kγ revealed that these mice maintained similar body weights and insulin levels as controls but showed improved insulin tolerance and reduced β-cell apoptosis.
- The findings suggest that PI3Kγ ablation could be beneficial for glucose intolerance in obesity through mechanisms related to adiposity and inflammation, providing new insights into its role in β-cell function.
Article Synopsis
- PI3Kγ is crucial for recruiting leukocytes during inflammation and influences insulin resistance linked to diet-induced obesity.
- Its role in inflammation and metabolism is largely related to its activity in non-immune cells, affecting overall fat accumulation.
- Interestingly, while PI3Kγ aids neutrophil recruitment to fat tissue, it can also enhance proinflammatory gene expression in macrophages, which complicates its perceived role as a suppressor of macrophage activation.
Article Synopsis
- Obesity and insulin resistance are linked to oxidative stress, and JNK1 has been identified as a potential drug target for obesity and type 2 diabetes treatment.
- A study investigated the long-term effects of JNK1 inactivation in obese mice on glucose regulation and oxidative stress, revealing that JNK1(-/-) mice on a high-fat diet had decreased antioxidant gene expression and more oxidative damage in their skin.
- Despite the skin damage, JNK1 ablation provided significant metabolic benefits, such as reduced obesity, inflammation, and insulin resistance, suggesting that targeting JNK1 in specific tissues could offer a safer treatment approach.
Article Synopsis
- * Mice lacking the PER2 protein (Per2 (Brdm1)) show lower blood sugar levels, disrupted liver glycogen storage, and altered eating patterns compared to normal mice.
- * PER2 is vital for regulating enzymes involved in glycogen metabolism, suggesting it plays a key role in managing how the liver stores glucose during feeding and fasting times.
Adipose tissue (AT) has become accepted as a source of multipotent progenitor cells, the adipose stromal cells (ASCs). In this regard, considerable work has been performed to harvest and characterize this cell population as well as to investigate the mechanisms by which transplanted ASCs mediate tissue regeneration. In contrast the endogenous release of native ASCs by AT has been poorly investigated.
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