Influence of peri-arterial hepatic denervation on the glycemic response to exercise in rats

Lindfeldt, J.; Balkan, Börk; Dijk, van Jitse; Scheurink, Antonius; Åhrén, Bo; Steffens, A.B.

doi:10.1016/0165-1838(93)90377-7

Cited by 11 publications

(9 citation statements)

References 19 publications

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“…It seems from most studies that the counterregulatory reaction on hypoglycemia (insulin‐induced), exercise (swimming, running), and food deprivation is normal (Lindfeldt et al, 1993; Moore et al, 1993; Latour et al, 1995; Trabelsi et al, 1995; Wiersma et al, 1995; Jackson et al, 2000). These data suggest that afferent signaling from the liver is not required for the normal counterregulating response.…”

Section: Effect Of Hepatic Denervation In Experimental Animal Modelsmentioning

confidence: 99%

Transplanted liver: Consequences of denervation for liver functions

et al. 2004

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Following liver transplantation, all hepatic nerves are transected; thus, liver allografts are completely isolated from neural control of their hosts. Despite this absolute denervation, liver allograft function does not appear to be significantly impaired after successful transplantation. In experimental animal models, hepatic denervation has no major effects on bile acid production and biotransformation, while it increases blood pressure and salt retention; decreases the number of hepatic progenitor cells, cholangiocyte proliferation, and liver regeneration; and influences the hepatic microcirculation, diet behavior, and glycemic control. In humans, hepatic denervation after liver transplantation has no major deleterious effects on bile secretion, liver regeneration, and hepatic blood flow. Insulin resistance and postprandial hyperglycemia, changes in ingestion behavior, and reduced stimulation of hepatic progenitor cells in the canals of Hering are the major side effects of absent liver innervation. Despite these abnormalities, patients can lead a new life with improved quality of life. © 2004 Wiley-Liss, Inc. Key words: liver transplantation; denervation; function; hepaticLiver transplantation is the ultimate treatment for patients with acute fulminant and chronic liver failure. The results of liver transplantation are good, with a 1-year survival of 90 -95% and a 10-year survival of 50 -60%. Because of a shortage in cadaveric donors, living-related liver transplantation is a good option to overcome this problem.The autonomic nerves of the liver are formed by an anterior plexus (around the hepatic artery) and a posterior plexus (surrounds portal vein and bile duct). Parasympathetic nerves are derived from the vagus nerve and the sympathetic fibers from the celiac ganglion. Sensory nerve endings are present in the liver capsule, central veins, and bile ducts. Most of the afferent nerves from the liver run via the vagus and splanchnic nerves, but some also to the right phrenic nerve. The afferent nerves register information from nocireceptors, osmo-and baroreceptors, as well as ionic and metabolic receptors (Bathal and Grossman, 1999).Following liver transplantation, the hepatic nerves are inevitably transected below the porta hepatis or at the hepatoduodenal ligament; thus, liver allografts are completely isolated from the neural control of their hosts. Despite this absolute denervation, the liver allograft does not appear to be significantly compromised after successful transplantation. There is no obvious deficiency in the regulation of liver metabolism (production of proteins such as albumin and coagulation factors, metabolization) and bile production. At first blush, it seems that under normal circumstances, hormones and substrates reaching the liver by circulation are responsible for control of the organ function, and that the role of hepatic nerves is mainly restricted to situations of physiological stress.However, a more profound search revealed that hepatic denervation has a lot of consequences...

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Section: Effect Of Hepatic Denervation In Experimental Animal Modelsmentioning

confidence: 99%

Transplanted liver: Consequences of denervation for liver functions

et al. 2004

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“…Similarly, in swimming rats, the exercise‐induced increase in hepatic glucose formation was attributed primarily to an increase in glucagon secretion. Circulating adrenaline and hepatic nerves became important only if glucagon secretion was suppressed (Lindfeldt et al, 1993; Van Dijk et al, 1994). Dog and rat liver parenchyma is scarcely innervated.…”

Section: Sympathetic Control Of Hepatic Glucose Outputmentioning

confidence: 99%

Control of hepatocyte metabolism by sympathetic and parasympathetic hepatic nerves

Püschel

2004

Anat. Rec.

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More than any other organ, the liver contributes to maintaining metabolic equilibrium of the body, most importantly of glucose homeostasis. It can store or release large quantities of glucose according to changing demands. This homeostasis is controlled by circulating hormones and direct innervation of the liver by autonomous hepatic nerves. Sympathetic hepatic nerves can increase hepatic glucose output; they appear, however, to contribute little to the stimulation of hepatic glucose output under physiological conditions. Parasympathetic hepatic nerves potentiate the insulindependent hepatic glucose extraction when a portal glucose sensor detects prandial glucose delivery from the gut. In addition, they might coordinate the hepatic and extrahepatic glucose utilization to prevent hypoglycemia and, at the same time, warrant efficient disposal of excess glucose. Key words: glucose homeostasis; metabolic regulation; insulin sensitivityMore than any other organ, the liver contributes to the maintenance of the metabolic equilibrium of our body. Depending on the nutrient supply, it can shift from net glucose uptake and storage to net glucose output, thereby providing the energy source for those tissues that obligatorily depend on glucose. Liver also is a center of amino acid metabolism and ammonia detoxification, being unique in harboring the complete urea cycle. The rate of hepatic amino acid metabolization and urea formation varies widely, depending on the nutritional state. Besides the gut, the liver is the only organ that contains significant amounts of xanthinoxidase and thus can catalyze the last steps in purine catabolism. Liver is a key player in lipid metabolism, as it synthesizes and degrades lipoproteins and converts fatty acids to ketone bodies. In rodents but not normally in humans, it also synthesizes fatty acids from carbohydrates. Liver is an exocrine gland producing bile acids and it is the only significant site of cholesterol excretion. It is also the prime site of xenobiotic metabolism, chiefly allowing xenobiotic detoxification but also toxification. Finally, it is a control station of the hormone system; different hormones that control the intermediary metabolism are either degraded, activated, or synthesized in the liver. The metabolic pathways serving all these functions are tightly regulated and are subject to control by metabolite levels, circulating hormones, and hepatic nerves. The different levels of control are interrelated in many ways. This complex mode of regulation makes it difficult to discern the contribution of one particular branch of this control system. The role of hepatic nerves in the control of hepatic metabolism has often been disputed because no gross aberration of the metabolic homeostasis was observed when the nervous supply to the liver was interrupted by surgical or pharmacological means. However, although direct nervous control apparently contributes only subtle changes to the metabolic control in liver, it becomes increasingly evident that this fine tuning may ...

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“…hepatic denervation and adrenodemedullation studies in animals that have suggested the greater importance of Epi than NE in stimulating R a (23,44). One study of Epi infusion during exercise was performed on celiac ganglion-blocked and islet cell-clamped human subjects exercising at 74% V O 2 max .…”

mentioning

confidence: 99%

Epinephrine infusion during moderate intensity exercise increases glucose production and uptake

Kreisman

Mew

Arsenault

et al. 2000

American Journal of Physiology-Endocrinology and Metabolism

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The glucoregulatory response to intense exercise [IE, >80% maximum O(2) uptake (VO(2 max))] comprises a marked increment in glucose production (R(a)) and a lesser increment in glucose uptake (R(d)), resulting in hyperglycemia. The R(a) correlates with plasma catecholamines but not with the glucagon-to-insulin (IRG/IRI) ratio. If epinephrine (Epi) infusion during moderate exercise were able to markedly stimulate R(a), this would support an important role for the catecholamines' response in IE. Seven fit male subjects (26 +/- 2 yr, body mass index 23 +/- 0.5 kg/m(2), VO(2 max) 65 +/- 5 ml x kg(-1) x min(-1)) underwent 40 min of postabsorptive cycle ergometer exercise (145 +/- 14 W) once without [control (CON)] and once with Epi infusion [EPI (0.1 microg x kg(-1) x min(-1))] from 30 to 40 min. Epi levels reached 9.4 +/- 0.8 nM (20x rest, 10x CON). R(a) increased approximately 70% to 3.75 +/- 0.53 in CON but to 8.57 +/- 0.58 mg x kg(-1) x min(-1) in EPI (P < 0.001). Increments in R(a) and Epi correlated (r(2) = 0.923, P

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Influence of peri-arterial hepatic denervation on the glycemic response to exercise in rats

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Cited by 11 publications

References 19 publications

Transplanted liver: Consequences of denervation for liver functions

Transplanted liver: Consequences of denervation for liver functions

Control of hepatocyte metabolism by sympathetic and parasympathetic hepatic nerves

Epinephrine infusion during moderate intensity exercise increases glucose production and uptake

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