Glut-1 expression and its response to hypoglycemia in the embryonic mouse heart

Abstract

The embryonic heart depends on glucose during early organogenesis. Glut-1 functions in constitutive glucose uptake in adult tissues and is the predominant glucose transporter in embryonic and fetal tissues. This study focuses on Glut-1 expression in the heart during normal organogenesis using immunohistochemistry for Glut-1 distribution, Western analysis for Glut-1 protein levels, and reverse transcriptase polymerase chain reaction for Glut-1 mRNA levels. The role of Glut in glucose uptake response to hypoglycemia in the embryonic heart is evaluated using the Glut inhibitor cytochalasin B. Cardiac Glut-1 expression is also evaluated after in vitro hypoglycemic exposure. Glut-1 levels are highest on gestational days 9-10, intermediate on gestational day 10.5, and lowest on gestational days 11.5-13.5 in the normal embryonic heart. Cardiac Glut-1 mRNA levels similarly decline between gestational days 9.5 and gd 13.5. Cytochalasin B produces a dose-dependent decrease in glucose uptake in hearts exposed to hypoglycemia for 30 min or 6 h, implicating Glut in this response. Glut-1 protein expression is unchanged after 2 or 6 h but increased after 12 and 24 h of hypoglycemia in the gestational day 9.5 heart. Thus, Glut-1 expression is prominent in the embryonic heart and is correlated with changes in cardiac glucose requirements during normal organogenesis. Glut activity increases in response to acute hypoglycemia and the expression of Glut-1 increases in response to prolonged hypoglycemia. These results support the importance of Glut-1 during normal cardiogenesis and in response to hypoglycemia in the embryonic heart.

GLUT4, GLUT1, and GLUT8 are the dominant GLUT transcripts expressed in the murine left ventricle

“…The upregulation of both GLUT1 and GLUT3 in TG9 mice is consistent with prior reports of altered gene transcription during heart failure [39]. Both GLUT1 as well as GLUT3 are commonly found in high abundance in fetal tissues [40] and GLUT1 is the major GLUT expressed in the fetal heart [7]. The relative changes in mRNA transcript levels observed in the aortic banding model, however, demonstrate that pathologic cardiac hypertrophy is not necessarily accompanied by an increase in GLUT1 mRNA expression.…”

“…GLUT4, the canonical insulin-responsive glucose transporter, is the predominant GLUT expressed in the adult heart [6]. GLUT1 is a major GLUT transporter expressed in the fetal heart [7]. GLUT1 also increases in abundance in the adult heart in response to myocardial injury or stress [8,9].…”

Conditional ablation and recovery of forebrain neurogenesis in the mouse

“…4H, I; n=3 mice/group). Furthermore, we did not observe any differences in GFAP and Glut1 immunoreactivity in the DG amongst nestin-tk + and wild-type mice treated with GCV, suggesting that the loss of mitotically active precursors does not elicit frank gliosis or vascular changes in the hippocampus [not shown, (Latov et al, 1979; Smoak and Branch, 2000)]. Further supporting a lack of inflammatory response in nestin-tk + mice greated with GCV, we found no increase in activated microglia by ED-1 immunostaining except along the cannula track, and the degree was similar between treatment and control groups.…”

“…It recognizes both to the 55-kDa and 45-kDa forms of GLUT1 on Western blot and does not react to colorectal cancer controls, and recognizes GLUT1 in human, mouse and rat tissue (manufacturer’s information, (Smoak and Branch, 2000)). Antibody was used at 1:800 titer.…”

Quantitative Expression and Immunohistochemical Detection of Glucose Transporters, GLUT1 and GLUT3 in the Rabbit Placenta during Successful Pregnancy

“…Resemble tendencies were observed in the rat brain and mouse fetal heart [9,38]. The activity of glucose transport in the heart of mouse embryo increased as acute response to hypoglycemia with increase expression of GLUT1 protein, whereas the alteration of GLUT1 mRNA was not clearly detected.…”