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Figure 1 Key events in the clinical course, including the onset of complications and therapeutic interventions, are summarized in Figure 2

Thus, we hypothesise that visceral adipocytes in obese mice, maybe partly through the crosstalk with LAMs and partly by p53-driven transcriptional reprogramming, possess mechanisms to restrain catabolic stimuli upon IF

(1992): Prevention of learned helplessness: in vivo correlation with cortical serotonin

As more GLP-1 prescriptions are written to manage not just diabetes and cardiovascular disease but also obesity, a key question emerges: What is the role of patient engagement and chronic disease management when prescribing these drugs

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