PMID- 29855257
OWN - NLM
STAT- MEDLINE
DCOM- 20190507
LR  - 20190507
IS  - 1471-2202 (Electronic)
IS  - 1471-2202 (Linking)
VI  - 19
IP  - 1
DP  - 2018 May 31
TI  - Altered functional connectivity of the default mode network by glucose loading in 
      young, healthy participants.
PG  - 33
LID - 10.1186/s12868-018-0433-0 [doi]
LID - 33
AB  - BACKGROUND: The functional connectivity of the default mode network (DMN) 
      decreases in patients with Alzheimer's disease (AD) as well as in patients with 
      type 2 diabetes mellitus (T2DM). Altered functional connectivity of the DMN is 
      associated with cognitive impairment. T2DM is a known cause of 
      cognitive dysfunction and dementia in the elderly, and studies have established 
      that T2DM is a risk factor for AD. In addition, recent studies with positron 
      emission tomography demonstrated that increased plasma glucose levels decrease 
      neuronal activity, especially in the precuneus/posterior cingulate cortex 
      (PC/PCC), which is the functional core of the DMN. These findings prompt the 
      question of how increased plasma glucose levels decrease neuronal activity in the 
      PC/PCC. Given the association among DMN, AD, and T2DM, we hypothesized that 
      increased plasma glucose levels decrease the DMN functional connectivity, thus 
      possibly reducing PC/PCC neuronal activity. We conducted this study to test this 
      hypothesis. RESULTS: Twelve young, healthy participants without T2DM and insulin 
      resistance were enrolled in this study. Each participant underwent resting-state 
      functional magnetic resonance imaging in both fasting and glucose loading 
      conditions to evaluate the DMN functional connectivity. The results showed that 
      the DMN functional connectivity in the PC/PCC was significantly lower in the 
      glucose loading condition than in the fasting condition (P = 0.014). CONCLUSIONS: 
      Together with previous findings, the present results suggest that decreased 
      functional connectivity of the DMN is possibly responsible for reduced PC/PCC 
      neuronal activity in healthy individuals with increased plasma glucose levels.
FAU - Ishibashi, Kenji
AU  - Ishibashi K
AUID- ORCID: 0000-0002-4590-7146
AD  - Research Team for Neuroimaging, Tokyo Metropolitan Institute of Gerontology, 35-2 
      Sakae-cho, Itabashi-ku, Tokyo, 173-0015, Japan. ishibashi@pet.tmig.or.jp.
FAU - Sakurai, Keita
AU  - Sakurai K
AD  - Department of Diagnostic Radiology, Tokyo Metropolitan Geriatric Hospital, 35-2 
      Sakae-cho, Itabashi-ku, Tokyo, 173-0015, Japan.
FAU - Shimoji, Keigo
AU  - Shimoji K
AD  - Department of Diagnostic Radiology, Tokyo Metropolitan Geriatric Hospital, 35-2 
      Sakae-cho, Itabashi-ku, Tokyo, 173-0015, Japan.
FAU - Tokumaru, Aya M
AU  - Tokumaru AM
AD  - Department of Diagnostic Radiology, Tokyo Metropolitan Geriatric Hospital, 35-2 
      Sakae-cho, Itabashi-ku, Tokyo, 173-0015, Japan.
FAU - Ishii, Kenji
AU  - Ishii K
AD  - Research Team for Neuroimaging, Tokyo Metropolitan Institute of Gerontology, 35-2 
      Sakae-cho, Itabashi-ku, Tokyo, 173-0015, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180531
PL  - England
TA  - BMC Neurosci
JT  - BMC neuroscience
JID - 100966986
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Adult
MH  - Brain/*physiology
MH  - *Brain Mapping
MH  - Cognitive Dysfunction/physiopathology
MH  - Diabetes Mellitus, Type 2/physiopathology
MH  - Female
MH  - Glucose/*metabolism
MH  - Healthy Volunteers
MH  - Humans
MH  - Magnetic Resonance Imaging/methods
MH  - Male
MH  - Neural Pathways/*physiology
PMC - PMC5984391
OTO - NOTNLM
OT  - Default mode network
OT  - Glucose
OT  - Posterior cingulate
OT  - Precuneus
OT  - Resting-state functional MRI
EDAT- 2018/06/02 06:00
MHDA- 2019/05/08 06:00
PMCR- 2018/05/31
CRDT- 2018/06/02 06:00
PHST- 2017/12/11 00:00 [received]
PHST- 2018/05/24 00:00 [accepted]
PHST- 2018/06/02 06:00 [entrez]
PHST- 2018/06/02 06:00 [pubmed]
PHST- 2019/05/08 06:00 [medline]
PHST- 2018/05/31 00:00 [pmc-release]
AID - 10.1186/s12868-018-0433-0 [pii]
AID - 433 [pii]
AID - 10.1186/s12868-018-0433-0 [doi]
PST - epublish
SO  - BMC Neurosci. 2018 May 31;19(1):33. doi: 10.1186/s12868-018-0433-0.