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Obese NLRP12-deficient mice exhibit increased symptoms of type 2 diabetes and high circulating leptin levels

The chronic disease of type 2 diabetes mellitus (T2DM) accounts for 90% of overall diabetes cases worldwide since 2015. T2DM results in high blood glucose levels, insulin insensitivity, and a chronic pro-inflammatory state. The pro-inflammatory state is caused by cytokines such as IL-1β and IL-18 that are produced by adipose-infiltrating immune cells, such as macrophages. These macrophages have been directly linked to the development of insulin insensitivity in T2DM. Nod-like receptors, such as NLRP3, create the cascade of effects that result in the secretion of IL-1β and IL-18. Studies have identified NLRP3 as a key component that induces the metabolic inflammation and insulin insensitivity seen in T2DM. More recently, previous research showed that NLRP12-deficient mice exhibited diet-induced obesity and inflammation, and demonstrated that the mice experienced a worsening of all symptoms related to T2DM. This study takes a deeper look into these results in order to further characterize pathologic and inflammatory changes in NLRP12-deficient mice that were fed a high fat diet. We specifically quantified levels of leptin, a hormone that is responsible for regulating energy balance and plays a significant role in the immune system by upregulating the secretion of proinflammatory cytokines, such as IL-1β. Quantification of leptin levels demonstrated NLRP12-deficient mice present to have increased levels of leptin compared to wildtype mice.

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