PMID- 35364449
OWN - NLM
STAT- MEDLINE
DCOM- 20220503
LR  - 20220503
IS  - 1878-0334 (Electronic)
IS  - 1871-4021 (Linking)
VI  - 16
IP  - 4
DP  - 2022 Apr
TI  - Brain insulin resistance as a mechanistic mediator links peripheral metabolic 
      disorders with declining cognition.
PG  - 102468
LID - S1871-4021(22)00082-0 [pii]
LID - 10.1016/j.dsx.2022.102468 [doi]
AB  - BACKGROUND AND AIMS: Studies continue to investigate the underlying mechanism of 
      the association between the increased risk of different types of cognitive 
      decline and metabolic dysregulation. Brain insulin resistance (BIR) has been 
      suggested to explain this association. The vital role of insulin in the body has 
      been examined intensively and extensively; however, its role in the brain 
      requires further investigation. Herein, we confined our focus to summarize the 
      role of brain insulin signaling and the negative effect of dysmetabolism on 
      insulin functioning in the brain. METHODS: Published scientific manuscripts 
      between 1998 and 2020 that discussed the effect of selected metabolic disorder 
      conditions such as obesity, type 2 diabetes mellitus (T2DM), and high-fat diet 
      (HFD) on brain functions were reviewed. The main keywords used were insulin 
      resistance, brain insulin resistance, obesity, T2DM, and cognition. RESULTS: 
      Various metabolic disorders were linked to the increased risk of BIR, and was 
      suggested to increase the probability of cognition impairment occurrence. Several 
      proposed mechanisms explain this association among which insulin resistance and 
      hyperinsulinemia were primary factors attributed to an increased risk of BIR 
      among various metabolic disorders. CONCLUSIONS: Understanding the trajectory of 
      the association between metabolic disorders and alternation in cognition status 
      could expand our vision of those overlapping conditions and pave the road to both 
      treatment and preventative strategies for cognitive disorders.
CI  - Copyright (c) 2022. Published by Elsevier Ltd.
FAU - Al Haj Ahmad, Reem M
AU  - Al Haj Ahmad RM
AD  - Department of Nutrition and Food Technology, School of Agriculture, The 
      University of Jordan, Amman, Jordan. Electronic address: alhaj.reem@hotmail.com.
FAU - Ababneh, Nidaa A
AU  - Ababneh NA
AD  - Cell Therapy Center (CTC), The University of Jordan, Amman, Jordan. Electronic 
      address: nidaaanwar@gmail.com.
FAU - Al-Domi, Hayder A
AU  - Al-Domi HA
AD  - Department of Nutrition and Food Technology, School of Agriculture, The 
      University of Jordan, Amman, Jordan. Electronic address: h.aldomi@ju.edu.jo.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20220318
PL  - Netherlands
TA  - Diabetes Metab Syndr
JT  - Diabetes & metabolic syndrome
JID - 101462250
RN  - 0 (Insulin)
SB  - IM
MH  - Brain/metabolism
MH  - Cognition
MH  - *Diabetes Mellitus, Type 2/complications
MH  - Diet, High-Fat/adverse effects
MH  - Humans
MH  - Insulin/metabolism
MH  - *Insulin Resistance/physiology
MH  - Obesity/metabolism
OTO - NOTNLM
OT  - Brain insulin resistance
OT  - Cognition
OT  - Dementia
OT  - Hyperinsulinemia
OT  - Obesity
OT  - T3DM
COIS- Declaration of competing interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2022/04/02 06:00
MHDA- 2022/05/04 06:00
CRDT- 2022/04/01 20:14
PHST- 2021/09/05 00:00 [received]
PHST- 2022/03/14 00:00 [revised]
PHST- 2022/03/16 00:00 [accepted]
PHST- 2022/04/02 06:00 [pubmed]
PHST- 2022/05/04 06:00 [medline]
PHST- 2022/04/01 20:14 [entrez]
AID - S1871-4021(22)00082-0 [pii]
AID - 10.1016/j.dsx.2022.102468 [doi]
PST - ppublish
SO  - Diabetes Metab Syndr. 2022 Apr;16(4):102468. doi: 10.1016/j.dsx.2022.102468. Epub 
      2022 Mar 18.