Table 1.

Effects of GIP receptor agonism or antagonism on glycemic control, body weight, and energy balance in animal models of obesity and diabetes (modified according to Campbell and Nauck) (47, 49).

Experimental approach		Glycemic homeostasis		Body weight/energy household
Intervention regarding GIP receptor stimulation	Model	Glucose tolerance	Insulin resistance	Body weight	Energy intake	Energy expenditure
Antagonism	Prevention of diet-induced obesity and diabetes	↑	↓	↓↓	(↓)	0
	Treatment of pre-existent obesity and diabetes	↑↑	↓	(↓)	0-(↓)	0
Agonism	Prevention of diet-induced obesity and diabetes	0	0	0	0-(↓)	0
	Treatment of pre-existent obesity and diabetes	↑↑	(↓)	0-(↓)	0-(↓)	0

Prevention of diet-induced obesity: healthy, nonobese animals at baseline receiving experimental treatment while receiving a high-fat diet. Treatment of pre-existing obesity: animals with genetic mutations (ob/ob or db/db mice) causing obesity or high-fat diet-induced obesity at baseline. Agonism summarizes peptide GIP agonists, interventions leading to GIP hypersecretion, or antibody-mediated stimulation of GIP receptors; antagonism summarizes peptide GIP antagonists, interventions against K cells or GIP secretion, or specific antibodies either inactivating circulating GIP or GIP receptors. “(↑), ↑, ↑↑” trend or significant increment in this parameter (weak, intermediate, or strong effect); “(↓), ↓, ↓↓” trend or significant reduction in this parameter (weak, intermediate, or strong effect); 0, no obvious effect. Only patterns that are representative of all published studies in this category have contributed to the conclusions summarized in this table.