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Despite of adequate sample size after calculation, the metabolic responses to EGCG in those patients with type 2 diabetes were various

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However, in 2006 it became clear that GIP(3-42) does not function as a physiological antagonist in vivo as its maximal circulating levels are insufficient to elicit antagonistic effects ( At the same time, in 2002, Gipr knockout mice were found to be protected against both obesity and insulin resistance induced by high-fat feeding ( Also in 2002, a GIP analogue with an N-terminal substitution of glutamic acid in position 3 with proline (Pro3), was made as an attempt to prolong the GIP actions by protecting from DPP-4 degradation (66) ( Figure 1 )

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