PMID- 35582933
OWN - NLM
STAT- MEDLINE
DCOM- 20220929
LR  - 20221104
IS  - 2574-173X (Electronic)
IS  - 2574-173X (Linking)
VI  - 42
IP  - 3
DP  - 2022 Sep
TI  - Effects of high-fat diet on nutrient metabolism and cognitive functions in young 
      APPKI(NL-G-F/NL-G-F) mice.
PG  - 272-280
LID - 10.1002/npr2.12257 [doi]
AB  - 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 Abeta 
      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 APPKI(NL-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 
      APPKI(NL-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 APPKI(NL-G-F/NL-G-F) mice, whereas 
      impaired thermoregulation and shortage of alternative energy sources specifically 
      occurred in young APPKI(NL-G-F/NL-G-F) mice. However, HFD had no impact on the 
      cognitive function, Abeta 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 
      APPKI(NL-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.
CI  - (c) 2022 The Authors. Neuropsychopharmacology Reports published by John Wiley & 
      Sons Australia, Ltd on behalf of The Japanese Society of Neuropsychopharmacology.
FAU - Wang, Wei
AU  - Wang W
AUID- ORCID: 0000-0002-6718-4954
AD  - Department of Integrative Neuroscience, National Center for Geriatrics and 
      Gerontology, Aichi, Japan.
FAU - Tanokashira, Daisuke
AU  - Tanokashira D
AD  - Department of Integrative Neuroscience, National Center for Geriatrics and 
      Gerontology, Aichi, Japan.
FAU - Shibayama, Yudai
AU  - Shibayama Y
AD  - Department of Integrative Neuroscience, National Center for Geriatrics and 
      Gerontology, Aichi, Japan.
FAU - Tsuji, Ryuhei
AU  - Tsuji R
AD  - Department of Integrative Neuroscience, National Center for Geriatrics and 
      Gerontology, Aichi, Japan.
FAU - Maruyama, Megumi
AU  - Maruyama M
AD  - Department of Integrative Neuroscience, National Center for Geriatrics and 
      Gerontology, Aichi, Japan.
FAU - Kuroiwa, Chiemi
AU  - Kuroiwa C
AD  - Department of Integrative Neuroscience, National Center for Geriatrics and 
      Gerontology, Aichi, Japan.
FAU - Saito, Takashi
AU  - Saito T
AD  - Laboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama, 
      Japan.
FAU - Saido, Takaomi C
AU  - Saido TC
AD  - Department of Neurocognitive Science, Institute of Brain Science, Nagoya City 
      University Graduate School of Medical Sciences, Nagoya, Japan.
FAU - Taguchi, Akiko
AU  - Taguchi A
AUID- ORCID: 0000-0003-2893-8685
AD  - Department of Integrative Neuroscience, National Center for Geriatrics and 
      Gerontology, Aichi, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20220518
PL  - United States
TA  - Neuropsychopharmacol Rep
JT  - Neuropsychopharmacology reports
JID - 101719700
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Insulin Receptor Substrate Proteins)
SB  - IM
MH  - *Alzheimer Disease/etiology/metabolism
MH  - Amyloid beta-Peptides/metabolism
MH  - Animals
MH  - Cognition
MH  - *Diabetes Mellitus, Type 2/complications/metabolism
MH  - Diet, High-Fat
MH  - Disease Models, Animal
MH  - Insulin Receptor Substrate Proteins/metabolism
MH  - Mice
MH  - Nutrients
PMC - PMC9515707
OTO - NOTNLM
OT  - Alzheimer's disease
OT  - cognitive function
OT  - high-fat diet
OT  - hippocampus
OT  - insulin receptor substrate 1
OT  - knock-in mouse model
OT  - nutrient metabolism
OT  - type 2 diabetes mellitus
COIS- The authors declare no conflict of interest.
EDAT- 2022/05/19 06:00
MHDA- 2022/09/30 06:00
PMCR- 2022/05/18
CRDT- 2022/05/18 04:53
PHST- 2022/03/29 00:00 [revised]
PHST- 2021/12/23 00:00 [received]
PHST- 2022/04/16 00:00 [accepted]
PHST- 2022/05/19 06:00 [pubmed]
PHST- 2022/09/30 06:00 [medline]
PHST- 2022/05/18 04:53 [entrez]
PHST- 2022/05/18 00:00 [pmc-release]
AID - NPR212257 [pii]
AID - 10.1002/npr2.12257 [doi]
PST - ppublish
SO  - Neuropsychopharmacol Rep. 2022 Sep;42(3):272-280. doi: 10.1002/npr2.12257. Epub 
      2022 May 18.