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Journal of Parenteral and Enteral Nutrition
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IV Hypertonic Glucose Stimulates the Exocrine Pancreas in Rat

Bo-Guang Fan, MD, PhD* and Åke Andrén-Sandberg, MD, PhD{dagger}

From the * Center for Gastrointestinal Disease, Taizhou Hospital, Zhejiang Province, China; and the{dagger} Department of Surgery, Stavanger University Hospital, Stavanger, Norway

Correspondence: Bo-Guang Fan, MD, PhD, 415–418 Whitney Ave, Hamilton, L8S 2H8 Canada. Electronic mail may be sent to fanboguang{at}yahoo.com.

Background: Pancreatic atrophy and dysfunction resulting from parenteral nutrition (PN) may be explained by several mechanisms; one of the important factors is the nutrient in the circulation, which affects the pancreatic growth and secretion. The effect of nutrients on the pancreatic exocrine still has controversies. The aim of the present study is to better understand the effect of IV glucose on the exocrine pancreas stimulated by cholecystokinin during the parenterally fed condition. Methods: Two mixed solutions consisting of 30% and 50% glucose, respectively, were used. Thirty male Sprague-Dawley rats were randomly divided into 5 groups, including a control group; a freely fed group received cholecystokinin; 2 groups were infused with 30% and 50% glucose, and a group was infused with 50% glucose with cholecystokinin. The body weight and pancreatic contents were measured after 10 days. Results: The body weight in all groups was increased but lower than in the freely fed rats. IV glucose caused a decrease in the pancreatic weight, the amount of the pancreatic protein and DNA, and the level of amylase but elevated the level of trypsin in all treated groups. The enzymes were elevated after infusion of cholecystokinin with glucose, but they were lower than in freely fed animals with cholecystokinin. Compared with 30% glucose, 50% glucose elevated the level of amylase but did not affect the level of trypsin. Conclusions: IV glucose results in atrophy of the exocrine pancreas, elevates the amylase in pancreas, but suppresses the stimulatory effect of cholecystokinin on the exocrine pancreas.

The effects of parenteral nutrition (PN) are different from those of enteral nutrition in many aspects. As an example, long-term PN results in atrophy and dysfunction of the gastrointestinal (GI) tract, including pancreas.1–3 This is probably due to the lack of stimulation of the enterocytes, possibly leading to impairment of the GI endocrine function.4,5 Consequently, a decrease in the serum levels of several GI hormones occurs during PN.1 The pancreatic hypotrophy and dysfunction may be caused by several mechanisms during PN; one of the factors is nutrient in the circulation, which plays an important role in pancreatic secretion.6–10

Glucose as a main component in PN solutions is a strong stimulant for the endocrine pancreas, but there is still a controversy regarding its impact on the exocrine pancreas. Some results showed that the concentrated glucose given intravenously decreased output of the exocrine pancreas,4,5,11–15 whereas others reported that this macronutrient stimulated the GI tract secretion.16–18 Even though the possibility that IV glucose affects the exocrine pancreas is under debate and the results are contradictory,8,9 in our previous study,10 IV glucose had been shown to have a stimulatory function for amylase synthesis. The present study further demonstrated that a higher concentration of glucose stimulated more amylase and that the alteration of amylase level was related with the concentration of infused glucose. This may be of clinical importance because, for example, in patients with pancreatitis the stimulation of pancreatic secretion should be avoided.

Hormones are potential trophic agents for the pancreas. The main hormone known to exert stimulatory effects on the production of amylase and pancreatic growth in human and animals is cholecystokinin (CCK).7,19,20 Its stimulatory effects on the exocrine pancreas are fully functional under the enterally fed condition, whereas during the parenterally fed condition, the stimulatory effect of CCK needs to be explored. The present study, therefore, is to better understand the effect of IV glucose on the exocrine pancreas stimulated by CCK during the parenterally fed condition.


   METHODS
Top
 METHODS
RESULTS
 DISCUSSION
 CONCLUSIONS
 
Allocation of Animals
Thirty male Sprague-Dawley rats, weighting 210–220 g at the start of the experiment, were randomly divided into 5 groups, with 6 rats in each group: C (control group with free feeding, no PN), F + CCK (freely fed group with CCK infusion, no PN), 30G (PN group infused with 30% glucose), 50G (PN group infused with 50% glucose), and 50G + CCK (PN group infused with 50% glucose plus CCK infusion).

Surgical Procedure for PN
The rats intended for PN were intraperitoneally anesthetized with 5% chloral hydrate before the operation. The operation was performed under sterile conditions. A silicon-rubber catheter was inserted into the right external jugular vein, according to the Steiger et al21 technique. The catheter was delivered to the skull subcutaneously and connected to a swivel via a protective coil attached to the skin of the skull. The rats serving as controls underwent the same operation as the PN rats, but the right jugular vein was just ligated and simply cut, and no catheter was inserted. These animals were also connected to a swivel via a protective coil attached to the skin of the skull. Immediately after the surgery, all rats intended for PN were infused with 5% glucose solution at a speed of 1.5 mL/h for 24 hours, followed by PN solution at 250 mL/kg/d until just before killing. Control and fed rats were provided with free access to standard food pellets and tap water throughout the experiment. All animals were kept at the condition of a constant level of temperature, individually living in the metabolic cages, and a 12-hour day/night cycle was provided. The duration of the experiment was 10 days.

Infusion of CCK
Twelve rats, 6 PN/6 fed, received sulfated CCK-8 (Dojindo Laboratories, Kamimashiki-gun, Kumamoto, Japan) in a dose of 5 µg/kg/h for 10 days by subcutaneous infusion via osmotic minipumps (Charles River, Kent, UK) implanted into the neck of the animal.

Compositions in the PN Solutions
Two different solutions were prepared under sterile conditions; they contained 30% and 50% glucose, respectively, as main base of the individual solution. The other ingredients, such as minerals, vitamins, sodium chloride, and potassium, were in the same amount. All solutions did not contain the fat and amino acids.

Pancreas Sampling
At the end of the experiment, the rats were exsanguinated by aortal puncture under 5% intraperitoneal chloral hydrate anesthesia. Plasma was collected, frozen immediately, and stored at –20°C until further analysis. The whole pancreas was immediately dissected out in toto, fat and lymph nodes were cleaned away, and it was weighed. The pancreatic glands were frozen and stored at –70°C until further analysis.

Determination of Pancreatic Protein, DNA, Enzyme Levels and Water Content
The protein level was determined according to the method described by Lowry et al.22 DNA was extracted by a commercially available kit (Stratagene, La Jolla, CA). The amount of amylase was determined according to the Dahlquist23 method, and trypsin activity was estimated according to the method of Pelot and Grossman.24 The water content of each pancreas was measured by a freeze-drying technique.

Statistics Evaluation
Numerical data were expressed mean ± SEM as statistical differences. The significance of difference between groups was calculated using the Mann-Whitney U test, or p < .05 was statistically considered significant.


   RESULTS
Top
 METHODS
 RESULTS
DISCUSSION
 CONCLUSIONS
 
Body Weight
At the end of the experiment, all groups had increased weight, with no significant difference even though the group 30G had a smaller increase. The body weight in the group 30G was slightly lower than in the group 50G, but no significance was found between the 2 groups. CCK did not influence the body weight. No significant difference was detected between the studied and the control groups.

Pancreatic Wet Weight
Glucose infusion caused a decrease in total pancreatic wet weight. The pancreatic weight in the group 30G was not below that in the group 50G. CCK elevated the pancreatic weight in both the fed and glucose groups, but the increase in the glucose (50G + CCK) group was smaller than in the fed (F + CCK) group (Table I).


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  		TABLE I Effect of different concentrations of glucose with/without CCK infusion, compared with freely fed group with/without CCK, on pancreatic contents after 10 days of PN

 

Pancreatic Protein, DNA and Water
The concentration (mg per gram of pancreatic tissue) and total content (mg per whole pancreas) of the pancreatic protein were decreased in the 2 glucose groups (30G and 50G); CCK greatly elevated the concentration and content of the pancreatic protein in the fed (F + CCK) group and the content in the glucose (50G + CCK) group (Table I). IV glucose reduced the concentration and content of pancreatic DNA, whereas CCK infusion (50G + CCK) did not affect it. CCK greatly elevated DNA content in freely fed rats compared with the controls and 50G + CCK (Table I).


Figure 1
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  		FIGURE 1. Effect of glucose with/without CCK, compared with the freely fed group with/without CCK, on the content of pancreatic amylase after 10 days of glucose infusion. C, control group; F + CCK, freely fed plus CCK; 30G, 30% glucose; 50G, 50% glucose; 50G + CCK, 50% glucose plus CCK. *p < .05, {dagger}p < .01, ns, not significant. **On C bar = compared to G30 and G50; *on F + CCK bar = compared to 50G + CCK.

 
Pancreatic Amylase and Trypsin
After 10 days of glucose infusion, the total content (unit per whole pancreas) of amylase in pancreas were decreased; compared with group 30G, group 50G had an elevated content of amylase. The amylase content was not affected in group F + CCK, but it was reduced in group 50G + CCK (Figure 1). IV glucose increased the content of trypsin. CCK significantly increased the content of trypsin in the fed rats, but the increase was repressed by glucose infusion (50G + CCK; Figure 2).


Figure 2
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  		FIGURE 2. Effect of glucose with/without CCK, compared with the freely fed group with/without CCK, on the content of pancreatic trypsin after 10 days of glucose infusion. C, control group; F + CCK, freely fed plus CCK; 30G, 30% glucose; 50G, 50% glucose; 50G + CCK, 50% glucose plus CCK; *p < .05, {dagger}p < .01, ns, not significant. **On C bar = compared to G30 and G50; **on F + CCK bar = compared to 50G + CCK.

 

   DISCUSSION
Top
 METHODS
 RESULTS
 DISCUSSION
CONCLUSIONS
 
The chemical and physical stimuli exerted on the pancreas during the course of digestion are most important for the pancreatic integrity.25,26 Those stimulatory effects are mediated mainly by neural and hormonal pathways within the digestive tract.27 Several peptide hormones regulate pancreatic enzyme secretion and pancreatic growth. CCK is known as an important stimulator for the exocrine pancreas. The pancreatic atrophy seen during PN is the absence of CCK because the atrophy induced by starvation can be reduced and even reversed by hypercholecystokininemia.28 The release of CCK has been shown to be dependent on the stimulation of intraluminal factors,29 and consequently, in conditions of starvation or during a parenterally fed condition, there will be no such stimulated release. Even though the pancreatic integrity depends on such different factors, nutrients in the circulation are important factors. However, it has been controversial regarding the exocrine pancreas response to the parenteral nutrients per se, such as main nutrient glucose in the PN solution.16,18,30,31 In our experimental model, we have not studied the secretion of pancreatic juice into the duodenum or the composition of the juice, but only the effects of IV glucose on the pancreatic size, enzyme levels, and protein remaining in the pancreas.

Hypertonic glucose leads to a high insulin level in the blood.32 Insulin has been demonstrated to have a direct stimulatory effect on the biosynthesis of pancreatic amylase.33–36 Our previous study10 together with the present one demonstrated that a higher concentration of glucose stimulated more amylase and that the alteration of amylase level was related to the concentration of infused glucose. This may be due to a high insulin level in the blood during infusion of hypertonic glucose, which stimulates the exocrine pancreas.32,37,38 The effect of CCK on the pancreatic exocrine is potentiated by insulin,39 and when a high concentration of glucose is present, CCK releases and stimulates insulin secretion.40

On the other hand, the present study showed that in parenterally fed rats, CCK infusion caused mild elevation in pancreatic weight, but was much less effective than in enterally fed rats. This suggests that IV glucose suppresses the full stimulatory effect of CCK on the exocrine pancreas and that nutrients or other factors in the GI tract play an important role in maintaining normal pancreatic growth. This is consistent with the previous finding that IV nutrients weaken stimulatory effect of CCK on the exocrine pancreas.8

Under normal enterally fed condition, synthesis of the pancreatic enzymes is regulated by food constituents within the GI tract,41 and the enzyme secretory response is mediated by CCK and other hormones.42 However, during a parenterally fed condition, not all pancreatic enzyme levels change uniformly. The present study showed that IV glucose reduced the amylase level but increased the trypsin level. CCK has been believed to have a divergent effect on the synthesis of pancreatic amylase and trypsin.43,28 The release of trypsin and CCK is conditioned by each other, constituting a feedback mechanism.44–46 This divergent change in those 2 enzymes indicates that CCK alone does not affect the enzyme level but suggests that other factors are involved in the regulation of the enzyme level during a parenterally fed condition.


   CONCLUSIONS
Top
 METHODS
 RESULTS
 DISCUSSION
 CONCLUSIONS
 
In summary, enteral delivery of food arouses a series of different growth factors, gut peptides, and neural mechanisms, which cooperate in the absorption and use of nutrients. The lack of food passage in the digestive tract during a parenterally fed condition puts the digestive organs at rest. During such a condition, hypotrophy of the exocrine pancreas was seen along with unparalleled effects on the pancreatic amylase and trypsin, suggesting that several factors mediate the synthesis of the pancreatic enzymes. Glucose elevates amylase level, suggesting that the exocrine pancreas is stimulated by insulin. Further, IV glucose reduced the full stimulatory effect of CCK on the pancreatic exocrine, suggesting that the pancreatic exocrine is regulated by multiple factors, not by CCK alone.

The present study, therefore, concludes that IV infusion of hypertonic glucose causes an atrophy of the exocrine pancreas, represses the stimulatory effect of CCK on the exocrine pancreas, but has a stimulatory effect on the synthesis of amylase in the pancreas.

Received for publication March 15, 2005. Accepted for publication October 4, 2005.

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Journal of Parenteral and Enteral Nutrition, Vol. 30, No. 1, 40-44 (2006)
DOI: 10.1177/014860710603000140
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B.-G. Fan
Effects of Parenteral Nutrition on the Exocrine Pancreas in Response to Cholecystokinin
JPEN J Parenter Enteral Nutr, January 1, 2008; 32(1): 57 - 62.
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