scholarly journals Exercise Down-Regulates Hepatic Fatty Acid Synthase in Streptozotocin-Treated Rats

2001 ◽  
Vol 131 (9) ◽  
pp. 2252-2259 ◽  
Author(s):  
Russell G. Fiebig ◽  
John M. Hollander ◽  
Li Li Ji
1999 ◽  
Vol 87 (3) ◽  
pp. 1009-1015 ◽  
Author(s):  
Russel Fiebig ◽  
Mitchell T. Gore ◽  
Li Li Ji

The effect of an acute bout of exhaustive exercise on hepatic fatty acid synthase (FAS) gene expression was examined in rats. Female Sprague-Dawley rats (age 8 wk) were fasted for 48 h (F, n = 6), or fasted, refed a high-fructose diet for 6 h, and killed at rest (R, n = 6) or killed after running on a treadmill at 27 m/min and 5% grade for 88 ± 7 min (E, n = 6). Gel mobility shift assay indicated that R rats had twofold higher liver nuclear protein binding to oligonucleotides corresponding to the insulin responsive sequence (−71/−50) and carbohydrate response element (+283/+303) on the FAS promoter, compared with F rats. Exercise severely attenuated this binding in liver nuclear extracts to the levels seen in F rats. Competition and supershift experiments revealed that the bound protein complexes contained the upstream stimulatory factors. Nuclear run-on experiment revealed a 49-fold increase in transcription rate of the FAS gene in R vs. F rats, whereas exercise suppressed the transcription rate. FAS mRNA abundance and FAS enzyme activity were dramatically increased with refeeding but were unaltered by exercise. The results reveal that dietary induction of hepatic FAS is stimulated by increased nuclear protein binding to insulin responsive sequence and carbohydrate response element, whereas exhaustive exercise attenuates the binding, which may precede downregulation of FAS mRNA and enzyme synthesis reported in our previous work (M. A. Griffiths, R. Fiebig, M. T. Gore, D. H. Baker, K. Esser, L. Oscai, and L. L. Ji. J. Nutr. 126, 1959–1971, 1996).


Molecules ◽  
2020 ◽  
Vol 25 (16) ◽  
pp. 3656
Author(s):  
Dayoun Lee ◽  
Youngji Han ◽  
Eun-Young Kwon ◽  
Myung-Sook Choi

d-allulose is an uncommon sugar that provides almost no calories when consumed. Its sweetness is 70% that of sucrose. d-allulose is a metabolic regulator of glucose and lipid metabolism. However, few reports concerning its effect on diabetes and related metabolic disturbances in db/db mice are available. In this study, we evaluated d-allulose’s effect on hyperglycemia, hyperinsulinemia, diabetes and inflammatory responses in C57BL/KsJ-db/db mice. Mice were divided into normal diet, erythritol supplemented (5% w/w), and d-allulose supplemented (5% w/w) groups. Blood glucose and plasma glucagon levels and homeostatic model assessment (HOMA-IR) were significantly lower in the d-allulose group than in the normal diet group, and plasma insulin level was significantly increased. Further, d-allulose supplement significantly increased hepatic glucokinase activity and decreased hepatic phosphoenolpyruvate carboxykinase and glucose-6-phosphatase activity. Expression of glucose transporter 4, insulin receptor substrate 1, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha and AKT serine/threonine kinase 2 were also upregulated by d-allulose supplement in adipocyte and muscle. Finally, d-allulose effectively lowered plasma and hepatic triglyceride and free fatty acid levels, and simultaneously reduced hepatic fatty acid oxidation and carnitine palmitoyl transferase activity. These changes are likely attributable to suppression of hepatic fatty acid synthase and glucose-6-phosphate dehydrogenase activity. Notably, d-allulose also reduced pro-inflammatory adipokine and cytokine levels in plasma. Our results indicate that d-allulose is an effective sugar substitute for improving lipid and glucose metabolism.


1996 ◽  
Vol 28 (Supplement) ◽  
pp. 100
Author(s):  
R. Fiebig ◽  
M. Gore ◽  
L. L. Ji ◽  
M. A. Griffiths ◽  
K. Esser ◽  
...  

2008 ◽  
Vol 36 (01) ◽  
pp. 81-93 ◽  
Author(s):  
Myung-Sook Choi ◽  
Un Ju Jung ◽  
Hye-Jin Kim ◽  
Gyeong-Min Do ◽  
Seon-Min Jeon ◽  
...  

This study examined the effect of a Du-zhong (Eucommia ulmoides Oliver) leaf extract (0.175 g/100 g diet) that was supplemented with a high-fat diet (10% coconut oil, 0.2% cholesterol, wt/wt) on hyperlipidemic hamsters. Hamsters fed with Du-zhong leaf extract for 10 weeks showed a smaller size of epididymal adipocytes compared to the control group. The supplementation of the Du-zhong leaf extract significantly lowered the plasma levels of triglyceride, total cholesterol, LDL-cholesterol, non HDL-cholesterol, and free fatty acid, whereas it elevated the HDL-cholesterol/total cholesterol ratio and apolipoprotein A-I levels. The hepatic cholesterol concentration was lower in the Du-zhong group than in the control group. The plasma total cholesterol concentration was positively correlated with hepatic HMG- CoA reductase activity (r = 0.547, p < 0.05) and hepatic cholesterol concentration (r = 0.769, p < 0.001). The hepatic fatty acid synthase and HMG- CoA reductase activities were significantly lowered by a Du-zhong leaf extract supplement in high fat-fed hamsters. Hepatic fatty acid synthase activity was positively correlated with plasma fatty acid concentration (r = 0.513, p < 0.05) that was lower in the Du-zhong group. These results demonstrate that the Du-zhong leaf extract exhibits antihyperlipidemic properties by suppressing hepatic fatty acid and cholesterol biosynthesis with the simultaneous reduction of plasma and hepatic lipids in high fat-fed hamsters.


1994 ◽  
Vol 87 (4) ◽  
pp. 441-446 ◽  
Author(s):  
K. J. Simpson ◽  
S. Venkatesan ◽  
T. J. Peters

1. Chronic alcohol feeding with a low-fat diet (4.4% total calories) produced a two- to three-fold increase in hepatic triacylglycerol and esterified cholesterol compared with pair-fed low-fat diet controls. Plasma lipids were similar in both groups. 2. Hepatic fatty acid synthesis rates measured in vivo with 3H2O were significantly lower in the alcohol-fed animals than in controls. Activities of hepatic fatty acid synthase (EC 2.3.1.85) and acetyl-CoA carboxylase (EC 6.4.1.2) were reduced in the alcohol-fed rats. 3. These results indicate that enhanced hepatic fatty acid synthesis does not occur in rats fed alcohol and a low-fat diet for 4 weeks, and is thus not implicated in the pathogenesis of alcohol-induced fatty liver.


1996 ◽  
Vol 28 (Supplement) ◽  
pp. 99
Author(s):  
L. L. Ji ◽  
R. Fiebig ◽  
M. Gore ◽  
M. A. Griffiths ◽  
K. Esser ◽  
...  

1987 ◽  
Vol 73 (2) ◽  
pp. 159-163 ◽  
Author(s):  
S. Venkatesan ◽  
R. J. Ward ◽  
T. J. Peters

1. Liver slices from chronically alcohol-fed rats incubated with 3H2O showed less than half the fatty acid synthesis rates of pair-fed controls. Addition of 50 mmol/l ethanol or of 10 mmol/l lactate and 1 mmol/l pyruvate to the incubation medium did not alter the fatty acid synthesis rates in either groups. Hepatic fatty acid synthesis rates measured in vivo with 3H2O were also significantly reduced in alcohol-fed rats. 2. Time-course experiments showed that after 1 week on the ethanol diet hepatic fatty acid synthesis rates in vitro were similar to control rats, although the liver triacylglycerol content was significantly increased. From the second week of feeding, fatty acid synthesis rates were significantly lower in alcohol-fed rats and the liver triacylglycerol content progressively increased compared with controls. 3. Fatty acid synthase activity in liver cytosolic fractions were similar to controls in the alcohol-fed group after 1 week of feeding but were significantly lower in alcohol-fed rats from the second week onwards. 4. These results indicate that hepatic triacylglycerol accumulation after alcohol feeding is not due to increased fatty acid synthesis. The reduced fatty acid synthesis observed is a consequence of triacylglycerol accumulation.


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