Impact of intraportal N[omega ]-nitro-L-arginine infusion on hepatic glucose metabolism in total parenteral nutrition-adapted dogs: Interaction with infection

Metabolism ◽  
2002 ◽  
Vol 51 (3) ◽  
pp. 274-283 ◽  
Author(s):  
Sheng-Song Chen ◽  
Christine M. Donmoyer ◽  
Joseph Ejiofor ◽  
Juli McCay ◽  
Richard Archuletta ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Parenteral Nutrition ◽  
Total Parenteral Nutrition ◽  
Arginine Infusion ◽  
Hepatic Glucose Metabolism ◽  
Hepatic Glucose

scholarly journals Hepatic and muscle glucose metabolism during total parenteral nutrition: impact of infection

1998 ◽  
Vol 275 (5) ◽  
pp. E763-E769 ◽  
Author(s):  
Owen P. McGuinness ◽  
Christine Donmoyer ◽  
Joseph Ejiofor ◽  
Suzanne McElligott ◽  
D. Brooks Lacy
Keyword(s):  
Glucose Metabolism ◽  
Parenteral Nutrition ◽  
Glucose Uptake ◽  
Total Parenteral Nutrition ◽  
Vena Cava ◽  
Glucose Disposal ◽  
Peripheral Tissues ◽  
Hepatic Glucose ◽  
Hepatic Glucose Uptake ◽  
The Impact

We examined the impact of infection on hepatic and muscle glucose metabolism in dogs adapted to chronic total parenteral nutrition (TPN). Studies were done in five conscious chronically catheterized dogs, in which sampling (artery, portal and hepatic vein, and iliac vein), infusion catheters (inferior vena cava), and Transonic flow probes (hepatic artery, portal vein, and iliac artery) were implanted. Fourteen days after surgery, dogs were placed on TPN. After 5 days of TPN, an infection was induced, and the TPN was continued. The balance of substrates across the liver and limb was assessed on the day before infection ( day 0) and 18 ( day 1) and 42 h ( day 2) after infection. On day 0, the liver was a marked net consumer of glucose (4.3 ± 0.6 mg ⋅ kg−1⋅ min−1) despite near normoglycemia (117 ± 5 mg/dl) and only mild hyperinsulinemia (16 ± 2 μU/ml). In addition, the majority (79 ± 13%) of the glucose taken up by the liver was released as lactate (34 ± 6 μmol ⋅ kg−1⋅ min−1). After infection, net hepatic glucose uptake decreased markedly on day 1(1.6 ± 0.9 mg ⋅ kg−1⋅ min−1) and remained suppressed on day 2 (2.4 ± 0.5 mg ⋅ kg−1⋅ min−1). Net hepatic lactate output also decreased on days 1 and 2 (15 ± 5 and 12 ± 3 μmol ⋅ kg−1⋅ min−1, respectively). This occurred despite increases in arterial plasma glucose on days 1 and 2 (135 ± 9 and 144 ± 9 mg/dl, respectively) and insulin levels on days 1 and 2 (57 ± 14 and 34 ± 9 μU/ml, respectively). In summary, the liver undergoes a profound adaptation to TPN, making it a major site of glucose disposal and conversion to lactate. Infection impairs hepatic glucose uptake, forcing TPN-derived glucose to be removed by peripheral tissues.

Lack of effect of parathyroid hormone on hepatic glucose metabolism in the dog

Metabolism ◽  
1981 ◽  
Vol 30 (5) ◽  
pp. 469-475 ◽  
Author(s):  
S. Bevilacqua ◽  
E. Barrett ◽  
E. Ferrannini ◽  
R. Gusberg ◽  
A. Stewart ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Glucose Metabolism ◽  
Hepatic Glucose Metabolism ◽  
Hepatic Glucose

scholarly journals Lack of skeletal muscle IL-6 influences hepatic glucose metabolism in mice during prolonged exercise

2017 ◽  
Vol 312 (4) ◽  
pp. R626-R636 ◽  
Author(s):  
Lærke Bertholdt ◽  
Anders Gudiksen ◽  
Camilla L. Schwartz ◽  
Jakob G. Knudsen ◽  
Henriette Pilegaard
Keyword(s):  
Skeletal Muscle ◽  
Glucose Metabolism ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Prolonged Exercise ◽  
Hepatic Glycogen ◽  
Glucose Content ◽  
Hepatic Glucose Metabolism ◽  
Hepatic Glucose ◽  
Single Bout ◽  
Substrate Choice

The liver is essential in maintaining and regulating glucose homeostasis during prolonged exercise. IL-6 has been shown to be secreted from skeletal muscle during exercise and has been suggested to signal to the liver. Therefore, the aim of this study was to investigate the role of skeletal muscle IL-6 on hepatic glucose regulation and substrate choice during prolonged exercise. Skeletal muscle-specific IL-6 knockout (IL-6 MKO) mice (age, 12–14 wk) and littermate lox/lox (Control) mice were either rested (Rest) or completed a single bout of exercise for 10, 60, or 120 min, and the liver was quickly obtained. Hepatic IL-6 mRNA was higher at 60 min of exercise, and hepatic signal transducer and activator of transcription 3 was higher at 120 min of exercise than at rest in both genotypes. Hepatic glycogen was higher in IL-6 MKO mice than control mice at rest, but decreased similarly during exercise in the two genotypes, and hepatic glucose content was lower in IL-6 MKO than control mice at 120 min of exercise. Hepatic phosphoenolpyruvate carboxykinase mRNA and protein increased in both genotypes at 120 min of exercise, whereas hepatic glucose 6 phosphatase protein remained unchanged. Furthermore, IL-6 MKO mice had higher hepatic pyruvate dehydrogenase (PDH)Ser232 and PDHSer300 phosphorylation than control mice at rest. In conclusion, hepatic gluconeogenic capacity in mice is increased during prolonged exercise independent of muscle IL-6. Furthermore, Skeletal muscle IL-6 influences hepatic substrate regulation at rest and hepatic glucose metabolism during prolonged exercise, seemingly independent of IL-6 signaling in the liver.

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