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• W1938168986 abstract "Leptin resistance is one of the main challenges of obesity. To date, two levels of resistance have been identified, first a decreased rate of leptin uptake into the brain and secondly a diminished central response to leptin. New findings have identified the mechanisms of leptin transport and demonstrated that it can be rescued in obesity, but it did not overcome the problem of central resistance. Alteration in the actions of leptin following diet-induced obesity (DIO) appears to be a multifactorial condition. Several phosphatases are inhibiting leptin signaling pathways in a pathological way. Besides, hypothalamic inflammation alters the neuronal circuits that control metabolism. Recent studies describing both mechanisms (inhibition of leptin signaling and inflammation), have provided key insights to potential new targets for treatment. However, recent data showing that DIO mice may conserve a cellular and physiological response to endogenous leptin, highlights the need to redefine the concept of “leptin resistance”." @default.
• W1938168986 created "2016-06-24" @default.
• W1938168986 creator A5076549817 @default.
• W1938168986 creator A5084320835 @default.
• W1938168986 date "2015-10-01" @default.
• W1938168986 modified "2023-10-05" @default.
• W1938168986 title "New insights in leptin resistance mechanisms in mice" @default.
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• W1938168986 doi "https://doi.org/10.1016/j.yfrne.2015.09.004" @default.
• W1938168986 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26410445" @default.
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