Glucose homeostasis during exercise in humans with a liver or kidney transplant

Kjær, Michael; Keiding, Susanne; Engfred, K.; Rasmussen, K; Sonne, B.; Kirkegård, P.; Galbo, H.

doi:10.1152/ajpendo.1995.268.4.e636

Cited by 40 publications

(44 citation statements)

References 21 publications

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“…Some data have been interpreted as inconsistent with the hypothesis of circulating catecholamine mediation of R a in IE (18,(25)(26)(27)(28)(29). Many of these may be explained by the absolute intensity of the exercise studied being lower than that which we hypothesize as the threshold above which the catecholamines become key regulators.…”

Section: Discussionmentioning

confidence: 66%

“…However, the subjects were exercising at Ͻ75% V O 2max , and R a increased only threefold. Another study (29) showed no significant attenuation of R a in subjects who had undergone liver transplantation, exercising at 82% V O 2max. However, the absolute intensity was quite low (only 68 vs. 108 W in our CCI subjects and ϳ260 W in our subjects exercising at 87% V O 2max [10]).…”

Section: Discussionmentioning

confidence: 92%

“…Our previous results have been consistent with plasma catecholamines being the primary mediators of this response (5,6,9,10,22,23), although a clear cause-effect relationship had not been established. Thus, this hypothesis has remained controversial (18,(25)(26)(27)(28)(29). Our recent work suggests that alone, Epi (22) and NE (23) are each capable of producing a portion of the IE R a response.…”

Section: Discussionmentioning

confidence: 99%

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Combined Infusion of Epinephrine and Norepinephrine During Moderate Exercise Reproduces the Glucoregulatory Response of Intense Exercise

et al. 2003

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Intense exercise (IE) (>80% V O 2max ) causes a seven-to eightfold increase in glucose production (R a ) and a fourfold increase in glucose uptake (R d ), resulting in hyperglycemia, whereas moderate exercise (ME) causes both to double. If norepinephrine (NE) plus epinephrine (Epi) infusion during ME produces the plasma levels and R a of IE, this would prove them capable of mediating these responses. G lucoregulation during low-and moderate-intensity exercise is primarily mediated by an increase in the portal venous glucagon-to-insulin ratio (1), which stimulates hepatic glucose output, maintaining euglycemia largely through a feedback mechanism (2-4) that matches the increment to the increased requirements. However, in intense exercise (IE) 80% V O 2max , an up to eightfold increase in glucose production (R a ) and a rise in glycemia occur, but plasma insulin (immunoreactive insulin [IRI]) changes little and glucagon (immunoreactive glucagon [IRG]) increases less than twofold (5). It seems unlikely that such changes, even insofar as they reflect portal vein concentrations, would mediate the R a response in IE. Furthermore, the R a response was unaffected in islet cell clamp studies using somatostatin and exogenous hormone infusions, in which peripheral IRG-to-IRI ratios (representative of portal levels) were kept unchanged or even decreased (6).A "feedforward" control of R a during IE has been proposed (4,7). We (5) and others (7,8) have proposed that the rapid and marked catecholamine response of IE could be such a mechanism. Plasma norepinephrine (NE) and epinephrine (Epi) concentrations both increase 15-fold, and we have demonstrated highly significant correlations of both with R a during IE (5). We recently found that the patterns of responses of plasma catecholamines and R a persist in glucose-infused subjects (9) and in the postprandial state (10). These are situations in which endogenous R a suppression from hyperinsulinemia must be overcome, the latter being the situation under which most IE is performed. In contrast, at lower-intensity exercise, attenuation or prevention of the R a increment occurs with exogenous glucose infusion (2)(3)(4)11,12).Catecholamine infusions stimulate R a in both dogs (13-15) and humans (16 -21). Most of these studies involved only Epi and were done at rest. Although some (16,19) produced Epi levels comparable to those of IE, the 1.5-to 2.5-fold increments in R a were considerably smaller. One study of Epi infusion during exercise was performed on celiac-ganglion-blocked and islet cell-clamped human subjects exercising at 74% V O 2max . Epi was doubled, to concentrations typical of IE, causing a further increment in R a over that of the exercise alone (18). Another study (17) with Epi infusion during 40% V O 2max exercise suggested that Epi contributes to, but does not fully account for, the R a increment of IE. Our recent studies of Epi (22) or NE (23) infusions during 50% V O 2max exercise suggest that plasma levels of each could provide a sizable contribution toward the...

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Section: Discussionmentioning

confidence: 66%

Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

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Combined Infusion of Epinephrine and Norepinephrine During Moderate Exercise Reproduces the Glucoregulatory Response of Intense Exercise

et al. 2003

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“…The onset of exercise causes an increase in sympathetic activity that correlates with an increase in R a . However, studies designed to assess the role of sympathetic drive to the liver in the stimulation of R a , using chronic denervation (8), local hepatic adrenergic blockade (9,10), and liver transplant patients (presumably free of sympathetic innervation to the liver) (11), have been uniformly negative. Nevertheless, studies performed in humans using the pancreatic clamp technique and combined ␣-and ␤-adrenergic blockade suggest that epinephrine may prevent overt hypoglycemia during moderate exercise (12).…”

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confidence: 99%

Prevention of Overt Hypoglycemia During Exercise

Coker

Koyama²,

Denny³

et al. 2002

Diabetes

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These studies were conducted to determine the magnitude and mechanism of compensation for impaired glucagon and insulin responses to exercise. For this purpose, dogs underwent surgery >16 days before experiments, at which time flow probes were implanted and silastic catheters were inserted. During experiments, glucagon and insulin were fixed at basal levels during rest and exercise using a pancreatic clamp with glucose clamped (PC/GC; n ‫؍‬ 5), a pancreatic clamp with glucose unclamped (PC; n ‫؍‬ 7), or a pancreatic clamp with glucose unclamped ؉ intraportal propranolol and phentolamine hepatic ␣-and ␤-adrenergic receptor blockade (PC/HAB; n ‫؍‬ 6). Glucose production (R a ) was measured isotopically. Plasma glucose was constant in PC/GC, but fell from basal to exercise in PC and PC/HAB. R a was unchanged with exercise in PC/GC, but was slightly increased during exercise in PC and PC/ HAB. Despite minimal increases in epinephrine in PC/ GC, epinephrine increased approximately sixfold in PC and PC/HAB during exercise. In summary, during moderate exercise, 1) the increase in R a is absent in PC/GC; 2) only a moderate fall in arterial glucose occurs in PC, due to a compensatory increase in R a ; and 3) the increase in R a is preserved in PC/HAB. In conclusion, stimulation of R a by a mechanism independent of pancreatic hormones and hepatic adrenergic stimulation is a primary defense against overt hypoglycemia. Diabetes

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“…Provision of a functional hepatic parenchyma has indeed been shown to restore many major metabolic functions of the liver. [13][14][15] The normal liver innervation, however, is irreversibly lost in the process of liver transplantation, which may possibly have unrecognized functional consequences. Liver transplant recipients frequently gain excessive amounts of body weight.…”

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confidence: 99%