ABSTRACT
Objective@#To explore the effect of long term aerobic exercise on microcirculation function and VO 2max of college students, and to explore the relationship between microcirculation function and VO 2max .@*Methods@#Seventy sports major college students were selected as the exercise group, 70 sedentary non sports major students were selected as the control group. PF6000 dual channel laser Doppler blood flow detector was used to assess the skin microcirculation function on the quadriceps femoris muscle of the subjects right lower limbs.The PFT Ergo cardiopulmonary function test system and the equipped power bicycle were used to measure the VO 2max of the subjects.@*Results@#The baseline value of MBP in the exercise group was significantly lower than that in the control group (6.5±1.8 vs. 8.1±2.5), but the microvascular reactivity(1 666.3±588.6 vs. 1 165.2±407.1) was significantly higher than that in the control group(t =-3.42，4.46， P <0.01). The absolute value of VO 2max (2 684.8±451.1 vs. 2 474.4±423.5) and relative value (42.7±4.3 vs. 35.1±4.8) in exercise group were significantly higher than those in control group( t =2.16，3.25， P < 0.01 ). Multiple regression showed that there was a positive correlation between microvascular reactivity and VO 2max (relative value) ( β = 0.40 , P =0.03), but no significant correlation between percutaneous oxygen partial pressure and VO 2max (relative value) ( β= 0.23 , P =0.19).@*Conclusion@#Long term physical exercise can decrease microcirculation perfusion volume, improve microvascular reactivity, percutaneous oxygen partial pressure among college students. Improvement of the microvascular reactivity may be a sport improving VO 2max (relative) one of the most important peripheral physiological mechanism.
ABSTRACT
Experimental and molecular epidemiological studies indicate important roles for adipose tissue or high-fat diet (HFD) in tumor growth and metastasis. Gastric cancer (GC) possesses a metastatic predilection for the adipocyte-rich peritoneum. However, the precise molecular relevance of HFD in the peritoneal metastasis of GC remains unclear. Here, we showed that HFD causes obvious fat accumulation and promotes peritoneal dissemination of GC in vivo. Peritoneum-derived adipocytes induces robust lipid droplet (LD) accumulation and fatty acid oxidation in GC cells through transcriptional upregulation of DGAT2 in a C/EBPα-dependent manner and prevents anoikis during peritoneal dissemination. Treatment of GC cells with FAs or coculture with adipocytes induces intracellular formation of LDs and production of NADPH to overcome oxidative stress in vitro. Importantly, overexpression of DGAT2 was identified as an independent predictor of poor survival that promotes lung and peritoneal metastasis of GC, and genetic or pharmacological inhibition of DGAT2, via disruption of lipid droplet formation in a lipid-rich environment, enhances the sensitivity of GC to anoikis in vitro and inhibits peritoneal metastasis in vivo. Overall, our findings highlight the notion that DGAT2 may be a promising therapeutic target in GC with peritoneal implantation and provide some evidence for uncovering the link between obesity and tumor metastasis.
