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    • Fig A demonstrates the body weight gain

    2022-05-19

    Fig. 2A demonstrates the body weight gain of the pregestational females. High-fat diet in wild-type mice increased body weight in 2 weeks and sustained this increase over 8 weeks. A similar effect was noted in glut3 mice in response to a high-fat diet. Fig. 2B depicts fat and muscle mass as assessed by quantitative nuclear magnetic resonance (NMR). Skeletal muscle mass did not change in response to a high-fat diet in both the genotypes. In contrast, the fat mass increased fourfold in the wt mice and only twofold in the glut3 mice. Table 1 depicts organ weights in the four experimental groups. No major changes were observed except in white adipose tissue which increased in response to the high-fat diet in both genotypes. Fig. 3A demonstrates the glucose tolerance tests in pregestational females. On a regular chow diet, both genotypes are glucose tolerant, mimicking each other. In response to a high-fat diet, both genotypes became glucose intolerant during the first phase between 30 and 60 min. Fig. 3B shows the insulin tolerance tests which revealed that the glut3 mice maintained on a regular chow diet were insulin sensitive in comparison to the wt mice on a regular chow diet. This difference is seen only in the upswing upon the return of glucose concentrations to baseline from the insulin induced nadir. This swift increase toward normalcy may reflect counterregulatory hormonal action. This is despite the glut3 female mice demonstrating higher baseline plasma glucose concentrations compared to the wild-type mice, when both genotypes were maintained on a regular chow diet. The wild-type mice on a high-fat diet revealed the absence of insulin resistance. The glut3 mice on a high-fat diet lost this early return to baseline exhibited by this BADGE on a regular chow diet, demonstrating relatively more insulin resistance when compared to the glut3 mice on a chow diet. Assessment of the plasma lipid profile revealed an increase in total cholesterol and high-density lipoprotein in both genotypes fed a high-fat diet. Additionally, a diminution in plasma triglycerides was noted in both these high-fat-diet-fed genotypes. No change in unesterified cholesterol and free fatty acids was noted, although a trend toward a decline was seen particularly in the wild-type genotype on a high-fat diet (Table 2). In Fig. 4A, at postnatal (PN) 1 day, the offspring revealed a reduction in body weight in response to maternal high-fat diet when compared to the chow-fed wt mice. In contrast, an increase in body weight at PN1 in glut3 mice exposed to a maternal high-fat diet vs. chow diet was evident. At PN21, while no difference between maternal high-fat and chow diet exposures in the wild-type offspring was seen, an increased body weight in response to maternal high-fat- vs. chow-diet-exposed glut3 mice (Fig. 4B) persisted. In addition, the day 21 glut3 mice displayed reduced body weight when compared to their age-matched wt mice when maintained on a chow diet. Fig. 5 demonstrates changes in gestational day 19 placental fatty acid transporter system. In Fig. 5A and B, an increase in fatty acid translocase (FAT)/CD36 was observed in response to a high-fat diet in the wild type with a trend in glut3 mice. In contrast, placental FATP1 trended toward a reduction in response to a high-fat vs. chow diet (Fig. 5A and C), while no change is seen with FATP4 (Fig. 5A and D) under the high-fat dietary condition in both genotypes. Fig. 6 depicts placental glucose transporter protein concentrations. Fig. 6A and B reveals an increase in placental Glut1 concentrations in response to a high-fat diet in wild-type and glut3 mice. In contrast, in Fig. 6A and C, no change was seen in wt placental Glut3 concentrations in response to a high-fat diet. However, the glut3 placentas revealed an increase in Glut3 concentrations in response to the high-fat diet. Thus, in glut3+/− mice, high-fat-diet-exposed placentas may have a cumulative effect of increased Glut1 and Glut3 proteins, while the wt may only exhibit the effect of increased Glut1 upon the developing fetus. This is reflected in the PN1 body weights of the offspring from the respective genotypes, with the glut3 demonstrating an increase while the wt expresses a diminution (Fig. 4A).