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Abstract Aim Type 2 diabetes mellitus (T2DM) is an increased risk factor for Alzheimer’s disease (AD); however, the relationship between the 2 conditions is controversial. High‐fat diet (HFD) causes cognitive impairment with/without Aβ accumulation in middle‐aged or aged transgenic (Tg) and knock‐in (KI) AD mouse models, except for metabolic disorders, which commonly occur in all mice types. Alternatively, whether HFD in early life has an impact on nutrient metabolism and neurological phenotypes in young AD mouse models is not known. In the present study, we examined the effects of HFD on young APPKINL‐G‐F/NL‐G‐F mice, one of the novel KI‐AD mouse models. Methods The mice were categorized by diet into 2 experimental groups, normal diet (ND) and HFD. Four‐week‐old wild‐type (WT) and APPKINL‐G‐F/NL‐G‐F mice were fed ND or HFD for 9 weeks. Both types of mice on ND and HFD were examined during young adulthood. Results HFD caused T2DM‐related metabolic disturbances in both young WT and APPKINL‐G‐F/NL‐G‐F mice, whereas impaired thermoregulation and shortage of alternative energy sources specifically occurred in young APPKINL‐G‐F/NL‐G‐F mice. However, HFD had no impact on the cognitive function, Aβ levels, and phosphorylation of hippocampal insulin receptor substrate 1 (IRS1) at all the 3 Ser sites in both types of mice. Conclusion HFD is effective in causing metabolic disturbances in young WT and APPKINL‐G‐F/NL‐G‐F mice but is ineffective in inducing neurological disorders in both types of mice, suggesting that the aging effects, along with long‐term HFD, facilitate neurological alterations.

Purpose: This study investigated the effects of 1400 mL intake of alkaline electrolyzed water (AEW) or purified water (PW) into which carbohydrate-electrolyte (CE) was dissolved on improving physiological responses during exercise under heat stress. Methods: This double-blinded, crossover randomized controlled trial included 10 male participants who completed two exercise trials in a hot environment (35 °C, ambient temperature, and 50% relative humidity) after consuming CE-dissolved PW (P-CE) or CE-dissolved AEW (A-CE). The exercise trial consisted of running for 30 min on a treadmill (at an intensity corresponding to 65% of heart rate reserve adjusted for heat stress conditions) and repeated sprint cycling (10 × 7-s maximal sprint cycling), with a 35-min rest interval between the two exercises, followed by a 30-min post-exercise recovery period. Before and after running, and after cycling, the participants drank P-CE (hydrogen concentration of 0 ppm, pH 3.8) or A-CE (0.3 ppm, pH 4.1). Blood samples were obtained before, during (rest interval between running and cycling), and post-exercise. Results: Repeated sprint performance and oxidative stress response did not differ between the P-CE and A-CE trials. A-CE consumption significantly attenuated the increase in blood lactate concentration during the running exercise but not during repeated sprint cycling under heat stress conditions. Conclusion: Our findings suggested that A-CE did not significantly affect repeated sprint performance; however, the attenuated elevation in blood lactate by A-CE ingestion implies a partial enhancement of endurance performance during submaximal exercise under heat stress.