PMID- 10644546
OWN - NLM
STAT- MEDLINE
DCOM- 20000306
LR  - 20171213
IS  - 0193-1849 (Print)
IS  - 0193-1849 (Linking)
VI  - 278
IP  - 1
DP  - 2000 Jan
TI  - Mice lacking insulin receptor substrate 4 exhibit mild defects in growth,
      reproduction, and glucose homeostasis.
PG  - E127-33
AB  - The insulin receptor substrates (IRSs) function in insulin signaling. Four
      members of the family, IRS-1 through IRS-4, are known. Previously, mice with
      targeted disruption of the genes for IRS-1, -2, and -3 have been characterized.
      To examine the physiological role of IRS-4, we have generated and characterized
      mice lacking IRS-4. Male IRS-4-null mice were approximately 10% smaller in size
      than wild-type male mice at 9 wk of age and beyond, whereas the female null mice 
      were of normal size. Breeding pairs of IRS-4-null mice reproduced less well than 
      wild-type mice. IRS-4-null mice exhibited slightly lower blood glucose
      concentration than the wild-type mice in both the fasted and fed states, but the 
      plasma insulin concentrations of the IRS-4-null mice in the fasted and fed states
      were normal. IRS-4-null mice also showed a slightly impaired response in the oral
      glucose tolerance test. Thus the absence of IRS-4 caused mild defects in growth, 
      reproduction, and glucose homeostasis.
FAU - Fantin, V R
AU  - Fantin VR
AD  - Department of Biochemistry, Dartmouth Medical School, Hanover, New Hampshire
      03755, USA.
FAU - Wang, Q
AU  - Wang Q
FAU - Lienhard, G E
AU  - Lienhard GE
FAU - Keller, S R
AU  - Keller SR
LA  - eng
GR  - DK-48216/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Physiol Endocrinol Metab
JT  - American journal of physiology. Endocrinology and metabolism
JID - 100901226
RN  - 0 (Blood Glucose)
RN  - 0 (Insulin)
RN  - 0 (Insulin Receptor Substrate Proteins)
RN  - 0 (Irs4 protein, mouse)
RN  - 0 (Phosphoproteins)
SB  - IM
MH  - Animals
MH  - Blood Glucose/*metabolism
MH  - Female
MH  - Glucose Tolerance Test
MH  - Growth/physiology
MH  - Homeostasis/physiology
MH  - Insulin/blood/physiology
MH  - Insulin Receptor Substrate Proteins
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout/genetics/*growth & development/*physiology
MH  - Phosphoproteins/genetics/*physiology
MH  - Reproduction/*physiology
EDAT- 2000/01/25 09:00
MHDA- 2000/03/11 09:00
CRDT- 2000/01/25 09:00
PHST- 2000/01/25 09:00 [pubmed]
PHST- 2000/03/11 09:00 [medline]
PHST- 2000/01/25 09:00 [entrez]
AID - 10.1152/ajpendo.2000.278.1.E127 [doi]
PST - ppublish
SO  - Am J Physiol Endocrinol Metab. 2000 Jan;278(1):E127-33. doi:
      10.1152/ajpendo.2000.278.1.E127.