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Before the company applied to the FDA for the drug to be approved for obesity, Knudsen and her colleagues 'developed a new methodology to show how [GLP-1] drugs exert their effect on the brain by working on the circumventricular organs and communicating further into the hypothalamus, among other effects.' This was designed to illustrate how GLP-1 worked in 'well- defined neurons in the hypothalamus, in the hindbrain, and in the reward centers.' Their rationale for developing the method was because 'It was very important to show that these medicines work on defined brain circuits and not ones that may be related to psychiatric or cardiovascular side effects, for example' (Nair

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Similarly, an animal model of diabetes-induced HF showed altered expression levels of copper transporter proteins and disturbed copper metabolism in rat cardiomyocytes (67)

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