Data on metabolic profile of insulin-degrading enzyme knockout mice

Insulin-degrading enzyme (IDE) degrades and inactivates bioactive peptides such as insulin. As insulin is a master regulator of glucose homeostasis, lack of IDE is expected to have a profound impact on both insulin and glucose levels. This article shares data on glucose and insulin homeostasis of control, heterozygous and knockout mice for Ide after 18 weeks of a normal chow diet. This data article is related to a research article entitled “Knockout of insulin-degrading enzyme leads to mice testicular morphological changes and impaired sperm quality” (Meneses et al., 2019).


Data
The data presented here are linked to a research article published separately by the same authors [1]. Here, we show the results regarding glucose and insulin fasting levels (Tables 1 and 2; Fig. 1A and B), glucose levels after a glucose bolus (Table 3; Fig. 1C), and the respective area under the curve (Table  4; Fig. 1D), which gives information about the capacity of the pancreas to release insulin in response to increased glucose levels [2]. Moreover, we also analyzed data regarding glucose levels after an insulin bolus (Table 5; Fig. 1E), and we have calculated the insulin resistance of these mice through the Homeostatic Model Assessment of Insulin Resistance (HOMA-IR; Table 6; Fig. 1F) [3].

Animals
Full body Ide heterozygous C57BL6/N mice were acquired from the European Mouse Mutant Archive (EMMA). After heterozygous breeding, wild type (WT), heterozygous (Het) and knockout (KO) mice were generated and maintained on a 12 h light/dark cycle with standard chow diet (Special Diets Specifications   Table 1 for raw data), fasting glucose levels (panel B; see Table 2 for raw data), blood glucose levels during an oral glucose tolerance test (OGTT; panel C; see Table 3 for raw data), the area under the glucose curve during the OGTT (panel D; see Table 4 for raw data), blood glucose levels during an insulin tolerance test (ITT; panel E; see Table 5 for raw data) and the Homeostatic Model Assessment of Insulin Resistance (HOMA-IR; panel F; see Table 6 for raw data) of heterozygous (Het) or knockout (KO) mice for Ide and wildtype (WT) mice. Results are expressed as mean ± SEM (n ¼ 5e8 for each condition). * À P < 0.05; ** À P < 0.01; *** À P < 0.001. Services, United Kingdom) and water ad libitum at Instituto Gulbenkian de Ciência (Oeiras, Portugal). Mice were monitored for body weight and blood glucose levels and all procedures followed ARRIVE guidelines and the Europeans laws (Directive 2010/63/EU) regarding the use of animals in research.

Oral glucose tolerance test
At 18 weeks old, and after an overnight fast, blood was collected from the mouse tail to measure blood glucose and insulin levels using a glucose meter and a mouse insulin ELISA kit (CrystalChem, Illinois, USA), respectively. Blood glucose levels were also measured 15, 30, 60 and 120 min after oral glucose administration (1.5 g/kg).

Insulin tolerance test
At 18 weeks old, and after 5 h of fasting, blood glucose levels were measured using a glucose meter before and 10, 20, 30, 45, 60, 90 and 120 min after insulin intraperitoneal injection (0.5 UI/kg). Table 3 Blood Glucose levels (mmol/L) during an oral glucose tolerance test (OGTT; 1.5 g glucose/Kg) of 18 weeks old wildtype (WT), heterozygous (Het) and knockout (KO) male mice for Ide. Corresponds to Fig. 1C. ns e non-significant. The bold indicates the most important data of the table, as it shows the mean and the SEM.

Table 4
Area under the curve (AUC) during an oral glucose tolerance test (OGTT; 1.5 g glucose/Kg) of 18 weeks old wildtype (WT), heterozygous (Het) and knockout (KO) male mice for Ide. Corresponds to Fig. 1D. ns e non-significant.

Statistical analysis
The statistical significance among the experimental groups was assessed by one-way ANOVA. Experimental data is shown as mean ± SEM. Statistical analysis was performed using GraphPad Prism 6 (GraphPad software, San Diego, CA, USA). p < 0.05 was considered significant.

Transparency document
Transparency document associated with this article can be found in the online version at https:// doi.org/10.1016/j.dib.2019.104023. The bold indicates the most important data of the table, as it shows the mean and the SEM.