. 2015 Nov 5;5:15942. doi: 10.1038/srep15942

Table 2. Comparison of the phenotypes among db/db mice, the Zucker rats and our Lepr ^−/− rats.

	db/db mice	Zucker rats	Lepr^−/−rats
Lepr disruption	Mutation at exon 19 g→t³⁵,³⁶ resulted in the deletion of the intracellular domain of Lepr.	Mutation at A⁸⁸⁰→C resulted in the replacement of Gln²⁶⁹→Pro³⁷, which does not affect the expression level of LEPR²⁶.	Lepr exon 4, 298-bp deletion and 4-bp insertion, generated stop codon, and leads the absence of LEPR expression.
Obesity	Appears at 1 month of age	Appears at 1 month of age	Appears at 1 month of age
Hyperphagia	Yes	Yes	Yes
Hyperglycemia	C57BL/6J background present with transient hyperglycemia; C57BL/KSJ background exhibit hyperglycemia, only survive to 10 months of age³².	Normal blood glucose levels¹⁰.	Mild hyperglycemia during 8 months of age.
Glucose intolerance	Yes	Yes, delayed onset of glucose intolerance²⁸.	Yes, appears as early as 2 months of age.
Diabetic complication	Renal lesion;³⁸ increased bone formation³.	Renal lesion; decreased bone volume²⁹.	Pancreas, liver and renal lesion; decreased bone volume.

Table 2. Comparison of the phenotypes among db/db mice, the Zucker rats and our Lepr −/− rats.