Effect of Acute Hyperglycaemia on Basal and Fat-Induced Exocrine Pancreatic Secretion in Humans

1997 ◽  
Vol 93 (6) ◽  
pp. 573-580 ◽  
Author(s):  
W. F. Lam ◽  
E. S. M. Muller ◽  
J. H. M. Souverijn ◽  
C. B. H. W. Lamers ◽  
A. A. M. Masclee
Keyword(s):  
Pancreatic Polypeptide ◽  
Healthy Subjects ◽  
Biliary Secretion ◽  
Exocrine Pancreatic Secretion ◽  
Indirect Measure ◽  
Acute Hyperglycaemia ◽  
Basal Period ◽  
Cholinergic Tone ◽  
Plasma Cholecystokinin ◽  
Hormonal Stimulus

1. We have investigated the effect of acute hyperglycaemia on pancreatico-biliary secretion in healthy subjects. Duodenal outputs of trypsin, lipase, amylase, bicarbonate and bilirubin were measured for 90 min under basal conditions and for 90 min in response to intrajejunal fat administration (1 g/h) on 2 separate days: during normoglycaemia (blood glucose 5 mmol/l) and during acute hyperglycaemia aimed at 15 mmol/l. Plasma cholecystokinin levels, as the major hormonal stimulus of pancreatic and biliary secretion, and plasma pancreatic polypeptide levels, as an indirect measure of vagal-cholinergic tone, were determined at regular intervals. 2. In the basal period pancreatico-biliary secretion was significantly (P < 0.05) reduced during hyperglycaemia compared with normoglycaemia. During normoglycaemia and hyperglycaemia intrajejunal fat significantly (P < 0.05) stimulated pancreaticobiliary secretion. However, during hyperglycaemia, fat-stimulated 90 min pancreatico-biliary secretion was significantly (P < 0.05) reduced compared with normoglycaemia: trypsin (23 ± 7 units versus 66 ± 20 units), lipase (36 ± 8 k-units versus 74 ± 18 k-units), amylase (8 ± 2 k-units versus 18 ± 5 k-units) and bilirubin (32 ± 8 μmol versus 71 ± 14 μmol). Plasma cholecystokinin levels increased significantly (P < 0.05) during fat administration and were not different between the two experiments. Plasma pancreatic polypeptide levels were significantly (P < 0.05) reduced during hyperglycaemia both in the basal period and during intrajejunal fat administration. 3. It is concluded that basal and fat-stimulated pancreatico-biliary secretion are significantly reduced during acute hyperglycaemia. Acute hyperglycaemia does not affect intrajejunal fat-stimulated cholecystokinin secretion. Acute hyperglycaemia inhibits basal and stimulated pancreatic polypeptide secretion suggesting vagal-cholinergic inhibition of pancreatico-biliary secretion during hyperglycaemia.

scholarly journals Impact of Growth Hormone Receptor Blockade on Substrate Metabolism during Fasting in Healthy Subjects

2009 ◽  
Vol 94 (11) ◽  
pp. 4524-4532 ◽  
Author(s):  
Louise Moller ◽  
Helene Norrelund ◽  
Niels Jessen ◽  
Allan Flyvbjerg ◽  
Steen B. Pedersen ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Insulin Sensitivity ◽  
Free Fatty Acids ◽  
Protein Metabolism ◽  
Healthy Subjects ◽  
Receptor Blockade ◽  
Substrate Metabolism ◽  
Gh Receptor ◽  
Basal Period ◽  
Igf I

Context: Experimental studies in GH-deficient patients and in healthy subjects receiving somatostatin-infusion suggest that GH is an important regulator of substrate metabolism during fasting. These models may not adequately reflect the selective effects of GH, and GH receptor (GHR) blockade offers a new model to define the metabolic role of GH. Objective: The aim of this study was to investigate the impact of GHR blockade on substrate metabolism and insulin sensitivity during fasting. Design: We conducted a randomized, placebo-controlled, crossover study in 10 healthy young men. Intervention: After 36 h of fasting with saline or pegvisomant (GHR blockade), the subjects were studied during a 4-h basal period and 2.5-h hyperinsulinemic euglycemic clamp. Main Outcome: We measured whole-body and forearm glucose, lipid, and protein metabolism, peripheral insulin sensitivity, and acyl and desacyl ghrelin. Results: GHR blockade significantly suppressed circulating free fatty acids (1226 ± 83 vs. 1074 ± 65 μmol/liter; P = 0.03) and ketone bodies (3080 ± 271 vs. 2015 ± 235 μmol/liter; P ≤ 0.01), as well as forearm uptake of free fatty acids (0.341 ± 0.150 vs. 0.004 ± 0.119 μmol/100 ml · min; P &lt; 0.01) and lipid oxidation (1.3 ± 0.1 vs. 1.2 ± 0.1 mg/kg · min; P = 0.03) in the basal period. By contrast, IGF-I levels in either serum or peripheral tissues were not impacted by GHR blockade, and protein metabolism was also unaffected. Basal glucose levels were elevated by GHR blockade, but insulin sensitivity was similar; this was associated with an increased acyl/desacyl ghrelin ratio. Conclusion: GHR blockade, without changes in circulating or tissue IGF-I levels, selectively suppresses lipid mobilization and oxidation after short-term fasting. This supports the notion that stimulation of lipolysis is a primary and important effect of GH. GH receptor blockade during fasting in healthy subjects suppresses lipid metabolism without a change in insulin sensitivity or protein metabolism.

A comparison of measurements of serum free T3 concentration by equilibrium dialysis, free T3 index, and T3: TBG ratio in thyroidal and non-thyroidal illnesses

1983 ◽  
Vol 103 (4) ◽  
pp. 501-508 ◽  
Author(s):  
Norimichi Konno ◽  
Takashi Nakazato ◽  
Kohji Hagiwara ◽  
Hideo Taguchi
Keyword(s):  
Serum Concentration ◽  
Healthy Subjects ◽  
Equilibrium Dialysis ◽  
Indirect Measure ◽  
Serum Free ◽  
Free T3 ◽  
Low Serum

Abstract. The present study was undertaken and compare the methods for measuring free T3 (FT3) by equilibrium dialysis, free T3 index (FT3I), and T3:T4-binding globulin (T3/TBG) in 40 healthy subjects, 26 patients with hyperthyroidism, 36 patients with hypothyroidism, 16 women in the 3rd trimester of pregnancy, 5 euthyroid subjects with low TBG, and 24 patients with non-thyroidal illnesses (NTI) with normal or low serum T3 concentration. Both FT3I and T3/TBG correlated significantly with FT3 (r = 0.98, P < 0.001 and r = 0.92, P< 0.001, respectively) when the data from all subjects were analyzed together. When each group was analyzed separately, FT3I still correlated significantly with FT3 in all groups (r = 0.67–0.97) except in the NTIs with low T3 (r = 0.18). The correlation of T3/TBG with FT3 was also significant in all groups (r = 0.60–0.88) other than the euthyroid with low TBG (r = 0.32) and NTIs with low T3 (r = 0.04). Both FT3I and T3/TBG values agreed well with the FT3 level in hyper- and hypothyroid subjects. In euthyroidism with abnormal TBG level, FT3I agreed well with FT3. However, T3/TBG gave a falsely lower FT3 when the TBG level was high, and a falsely higher FT3 when the TBG was low. In NTIs with normal T3, both FT3I and T3/TBG agreed well with FT3, but FT3I and T3/TBG values were all subnormal in NTIs with low T3, where FT3 ranged from normal to subnormal. These data suggest that 1) both FT3I and T3/TBG may be equally useful for an assessment of FT3 level in hyperand hypothyroidism, 2) FT3I may be superior to T3/TBG in euthyroidism with abnormal TBG concentration in serum, and 3) neither FT3I nor T3/TBG may be valid for an indirect measure of FT3 in NTIs with low serum concentration of T3.

Ascorbic Acid Attenuates the Haemodynamic Effects of Acute Hyperglycaemia in Healthy Subjects

2001 ◽  
Vol 100 (s44) ◽  
pp. 20P-20P
Author(s):  
BA Mullan ◽  
IS Young ◽  
CN Ennis ◽  
DR McCance
Keyword(s):  
Ascorbic Acid ◽  
Healthy Subjects ◽  
Haemodynamic Effects ◽  
Acute Hyperglycaemia

scholarly journals Pancreatic polypeptide release: Role of stimulants of exocrine pancreatic secretion in dogs

1984 ◽  
Vol 87 (3) ◽  
pp. 530-536 ◽  
Author(s):  
Christoph Beglinger ◽  
Ian L. Taylor ◽  
Morton I. Grossman ◽  
Travis E. Solomon
Keyword(s):  
Pancreatic Polypeptide ◽  
Pancreatic Secretion ◽  
Exocrine Pancreatic Secretion

Central cholinergic regulation of pancreatic polypeptide secretion in conscious dogs

1997 ◽  
Vol 154 (2) ◽  
pp. 311-317 ◽  
Author(s):  
M Okita ◽  
A Inui ◽  
S Baba ◽  
M Kasuga
Keyword(s):  
Food Intake ◽  
Pancreatic Polypeptide ◽  
Atropine Sulfate ◽  
Basal Secretion ◽  
Cholinergic Mechanisms ◽  
Glucose Levels ◽  
Plasma Pretreatment ◽  
Cephalic Phase ◽  
Cholinergic Tone ◽  
Blood Glucose Concentrations

Abstract The secretion of pancreatic polypeptide (PP) is regulated by fluctuations in blood glucose concentrations and food intake, in which vagal-cholinergic mechanisms play an important role, especially for the cephalic phase of PP secretion. In this study, we examined whether central cholinergic mechanisms are also important for PP secretion by relaying information in the brain to the vagus nerve and the muscarinic cholinergic receptors in the pancreas. Atropine sulfate (20–200 μg) was administered into the lateral cerebral ventricle and its effects on the basal secretion of PP as well as the secretions stimulated by insulin-induced hypoglycemia (Actrapid MC, 0·25 U/kg) and a mixed meal (243 kcal) were studied in seven dogs. Intralateral cerebroventricular (ILV) atropine (100 and 200 μg) abolished the fluctuations in basal PP secretion without appearing in the plasma. Pretreatment with 20, 100, and 200 μg ILV atropine significantly decreased the PP response to insulin-induced hypoglycemia, with the integrated PP response to 58, 32, and 26% of that of controls respectively. Atropine (100 μg ILV) significantly reduced the postprandial PP secretion in both the cephalic and the gastrointestinal phases, whereas increased insulin and glucose levels were unaffected. Centrally administered atropine was able to suppress the basal secretion of PP as well as the secretions stimulated by hypoglycemia and food intake. These findings suggest that (1) the spontaneous release of PP is governed by an oscillating, central cholinergic tone, and (2) the stimulating PP secretion is, at least in part, regulated by the central cholinergic system. Journal of Endocrinology (1997) 154, 311–317

Acute Rise of Pancreatic Polypeptide after Electroconvulsive Therapy

1982 ◽  
Vol 141 (1) ◽  
pp. 24-26 ◽  
Author(s):  
J. M. Allen ◽  
T. E. Adrian ◽  
P. A. Cramer ◽  
J. Steinert ◽  
S. R. Bloom
Keyword(s):  
Electroconvulsive Therapy ◽  
Pancreatic Polypeptide ◽  
Vagal Stimulation ◽  
Cholinergic Tone ◽  
Dramatic Rise

SummaryPlasma pancreatic polypeptide concentrations rise by 320±81 per cent following administration of electroconvulsive therapy. This rise is observed in the first ten minutes despite premedication of patients with 0.6 mg atropine. Pancreatic polypeptide release is dependent on cholinergic tone and is very sensitive to atropine. The dramatic rise in pancreative polypeptide observed following electroconvulsive therapy probably results from vagal stimulation and reflects insufficient atropine premedication.

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