Fat Metabolism in Three Forms of Obesity V. Hepatic Lipogenesis in Vitro

1955 ◽  
Vol 181 (3) ◽  
pp. 501-503 ◽  
Author(s):  
Jean Mayer ◽  
Norma C. Hagman ◽  
Norman B. Marshall ◽  
Anne Jones Stoops
1961 ◽  
Vol 200 (5) ◽  
pp. 1043-1046 ◽  
Author(s):  
Arliss Denyes ◽  
Joan D. Carter

When the hamster is exposed to cold (6 ± 1 C), there is a profound block in hepatic lipogenesis from C14-acetate within 48 hr. By 8 weeks of cold exposure this block has been repaired to 74% of the control value. During hibernation, which generally occurs after the 8th week, a block in lipogenesis is again present. By 6 hr of arousal, the degree of lipogenesis has been either slightly repaired or has returned almost to the 8-week level. Accompanying this block in lipogenesis is an increase in the production of C14O2 from C14-acetate in animals exposed to cold. In vitro addition of .02 m glucose did not stimulate lipogenesis in hepatic tissue of cold-exposed hamsters, except for a few of those animals aroused from hibernation for 6 hr. Addition of .02 m succinate in vitro did not increase lipogenesis or C14O2 production from C14-acetate. Fructose repaired the hepatic lipogenesis in all groups of cold-exposed hamsters. It was concluded that the cold-exposed and hibernating hamster has biochemical lesions involving the glucokinase reaction and some other step in the glycolytic pathways of the liver.


2021 ◽  
Author(s):  
Haifang Li ◽  
Xue Xiao ◽  
Geng Hu ◽  
Dalin He ◽  
Wenqian Zhang ◽  
...  

Abstract Multiwalled carbon nanotubes (MWCNTs) offer immense opportunities to deliver drug and biomolecules to targeted tissues. However, it’s unclear for us about their effects on fat metabolism. Here, we demonstrate that nitrogen-doped carboxylate-functionalized MWCNTs (N-MWCNTs) inhibit fat deposition both in vivo and in vitro primarily by suppressing adipogenesis. N-MWCNTs show good biocompatability in HEK293 mammalian cells. Intramuscular administration of N-MWCNTs does not affect the body weight gain and feed intake of mice, but reduces the fat mass. In in vitro-cultured adipocytes, N-MWCNTs suppress fat accumulation, accompanying with decreased and increased expression of adipogenic and lipolysis genes, respectively. Transcriptome analysis further certified the N-MWCNT alteration of fat metabolism-related genes. Interestingly, we observed the phagocytosis of N-MWCNTs by macrophage-like cells via TEM imaging. The mRNA sequencing data also showed remarkable variation of the genes involved in TLRs pathway, ultimately leading to down- or up-regulation of inflammatory factors, of which Tnfα, Il1, Il7, Il10, and Il12 are decreased, whereas Il6 and Il11 are increased. In conclusion, N-MWCNTs induce the production of inflammatory cytokines through immune responses, which trigger the reduction of fat deposition. These findings support the usage of N-MWCNTs as a promising delivery for anti-obesity agents.


1956 ◽  
Vol 186 (2) ◽  
pp. 190-192 ◽  
Author(s):  
W. F. Perry ◽  
Helen F. Bowen

The production of radioactive CO2 by intact and adrenalectomized rats given 1 C14 octanoic acid and the production of radioactive CO2 and radioactive acetoacetic acid by surviving liver slices from adrenalectomized and unoperated rats using 1 C14 octanoic acid as substrate have been studied. It was found that the CO2 production and acetoacetic acid production in vitro and CO2 production in vivo did not differ in the two types of animals. These results suggest that the adrenalectomized rat does not utilize fatty acids at a higher than normal rate and that the previously reported decreased incorporation of acetate into fatty acids by the liver slices from adrenalectomized rats is a reflection of decreased hepatic lipogenesis.


1980 ◽  
Vol 192 (1) ◽  
pp. 361-364 ◽  
Author(s):  
L Agius ◽  
D H Williamson

An intragastric load of medium- or long-chain triacylglycerols inhibited lipogenesis in lactating rat mammary gland in vivo by 82 or 89% respectively. This inhibition was reversed partially by insulin administration. Long-chain triacylglycerols inhibited hepatic lipogenesis in vivo but medium-chain triacylglycerols increased it 2-fold. Glucose utilization in vitro by mammary gland acini from triacylglycerol-fed rat was normal.


Author(s):  
P. Legrand ◽  
J. Mallard ◽  
M.A. Bernard-Griffiths ◽  
M. Douaire ◽  
P. Lemarchal

1983 ◽  
Vol 244 (5) ◽  
pp. E480-E486 ◽  
Author(s):  
B. Kalderon ◽  
J. H. Adler ◽  
E. Levy ◽  
A. Gutman

Synthesis of fatty acids was measured in the liver and in epididymal adipose tissue of sand rats and albino rats. In chow-fed sand rats the rate of hepatic lipogenesis, as measured by the incorporation of 3H2O into fatty acids, was four- to sevenfold higher than in albino rats and in sand rats on a low-calorie saltbush diet. The contribution of [14C]glucose to lipogenesis in sand rat liver was lower than in albino rats. In fed sand rats lipogenesis incorporating 3H2O was stimulated by casein but not by glucose. In adipose tissue, lipogenesis measured 1 h after administration of 3H2O was much lower in sand rats than in albino rats. In vitro incorporation of [14C]glucose or acetate into adipose tissue fatty acids was negligible. In adipose tissue, uptake of very-low-density lipoproteins (VLDL) and lipoprotein lipase activity were sevenfold higher than in albino rats. Activities of NADP-malate dehydrogenase, acetyl CoA carboxylase, and fatty acid synthetase were considerably higher in the liver of chow-fed sand rats than in albino rats. It was concluded that obesity in sand rats originates from hepatic lipogenesis without a significant contribution of local fatty acid synthesis in adipose tissue.


1984 ◽  
Vol 67 (4) ◽  
pp. 457-460
Author(s):  
Amal S. Al-Saadi ◽  
J. Stewart Orr ◽  
Anthony W. Goode ◽  
Mary C. Sugden

1. Lipogenic rates (measured with 3H2O) in hepatocytes from fed or starved euthyroid rats were similar in magnitude to those measured in livers in vivo. Hepatic lipogenesis in vivo in fed triiodothyronine (T3)-treated rats was greater than in fed control rats, but rates in vitro were only 16% of those of control rats. It is concluded that hepatic lipogenesis in vivo in T3-treated rats utilizes precursors from extrahepatic tissues. 2. Glycogen depletion of hepatocytes from fed control rats decreased lipogenesis, and rates were then similar to those in hepatocytes from fed T3-treated rats. Addition of lactate (2 mmol/l) and pyruvate (0.2 mmol/l) had little stimulatory effect on lipogenesis in hepatocytes from fed control rats, but increased lipogenesis in glycogen-depleted hepatocytes (by 86%), hepatocytes from starved rats (by 25%) and hepatocytes from T3-treated rats (by 60%). 3. In the presence of lactate and pyruvate, 3-mercaptopicolinate (3-MPA) (an inhibitor of gluconeogenesis) did not affect lipogenesis in hepatocytes from fed control rats but substantially increased lipogenesis in hepatocytes from starved euthyroid rats or fed hyperthyroid rats. Thus, in hepatocytes from starved euthyroid rats or fed hyperthyroid rats gluconeogenesis competes with lipogenesis for available precursors (lactate and pyruvate). In contrast, in fed rats carbon flux is predominantly towards lipogenesis. 4. Effects of 3-MPA in the presence of lactate and pyruvate were much less in glycogen-depleted cells from fed rats than in hepatocytes from starved or T3-treated rats. Thus glycogen depletion per se does not cause a redirection of carbon flux.


Sign in / Sign up

Export Citation Format

Share Document