Mean Plasma Glucagon Concentration Research Articles

Traditional versus agricultural lifestyle among Shuar women of the Ecuadorian Amazon: Effects on leptin levels

Leptin is a key biological marker related to energy balance and development of diabetes and cardiovascular diseases. Its levels are increased in populations with a high degree of the metabolic syndrome. Life history of evolution has, however, largely taken place under the ecological context of hunting and gathering. In this study, we explored whether the first steps of transition to sedentary agriculture involve a change of body composition, plasma leptin concentration, and markers of the metabolic syndrome. A total of 59 healthy Shuar Amerindian women living in 5 isolated communities in the Ecuadorian Amazonian rain forest were examined. Women (n = 33) from the largest and oldest community, Yuwientsa, who are more dependent on agriculture had higher fat mass (11.7 ± 3.3 v 14.5 ± 4.0 kg; P = .023) but the same body mass index (24.1 ± 2.7 v 23.1 ± 2.8 kg/m 2; not significant [NS]) and lean body mass (41.0 ± 5.0 v 40.2 ± 6.2 kg; NS) than women (n = 26) from the 4 traditional hunter/gather settlements. Furthermore, women from Yuwientsia had higher leptin (5.5 ± 3.1 v 4.1 ± 2.7 ng/mL; P = .021) and plasma insulin levels (49.8 ± 37.4 v 35.5 ± 12.7 pmol/L; P = .013). Homeostasis model assessment (HOMA) values (8.8 ± 4.8 v 6.1 ± 2.2; P = .004) and plasma triglyceride levels (2.3 ± 1.0 v 1.7 ± 0.6 mmol/L; P = .025) as markers of the metabolic syndrome were also increased in the Yuwientsa population. Mean plasma glucagon concentrations were not different between the groups. We conclude that body fat and levels of insulin and leptin are higher in the population more dependent on agriculture for living. In fact, the leptin concentrations from the 4 hunter/gather communities are the lowest mean value ever reported from a population of healthy females. As there are no genetic or biologic differences between the Shuar Indians from the 5 communities, we hypothesize that behavioral responses to a changing environment may be the key to the development of the metabolic syndrome and elevated plasma leptin concentrations.

The intravenous glucose tolerance test in water buffalo

Objective: The response to intravenous glucose loading in the buffalo using the intravenous glucose tolerance test (IGTT) was investigated to provide a reference for intravenous glucose injection in buffaloes. Method: Twelve healthy, fasted, male swamp buffaloes were divided into three groups. Group I: six buffaloes were given 50% glucose at a dosage of 1 g/kg body weight via the jugular vein. Group II: three buffaloes received normal saline. Group III: three buffaloes were not injected. Blood samples were taken from the opposite vein at 60 and 10 min pre-injection (pre60 and pre10), and at 1, 5, 10, 30, 60, 120, 180, 240, 300, 360 and 420 min post-glucose injection (PGI). Plasma glucose was analyzed by the oxidase method. Insulin and glucagon were soon determined with a human radioimmunoassay kit. The insulin (pmol/l)/glucose (mmol/l) ratios (IGR) were also calculated for each sampling time. Results: Mean plasma glucose, insulin and glucagon concentrations of buffaloes in groups II and III were similar at all the sampling times ( p>0.05) and the curves of the IGR for group II and group III were flat throughout. Group I Buffaloes showed an immediate 20 times increase in the mean plasma glucose concentration PGI, over the pre60 and pre10. The peak plasma insulin concentration occurred at 30 min PGI. The mean plasma glucose and insulin concentrations remained above pre-administration levels untill 420 min PGI ( p<0.05). However, the mean plasma glucagon concentrations were different only at 1 and 5 min PGI sampling times. The curve of the IGR for group I showed an initial decrease at 1 min PGI, and fluctuated from 10.18 to 25.55 for the remainder of the sampling period. The correlation analysis showed that the mean plasma glucose concentration was positively correlated with insulin level ( r=0.73, p<0.005), and significantly negatively correlated with mean plasma glucagon ( r=−0.58, p<0.05). The mean plasma insulin level did not show significant correlation with the glucagon ( r=0.06, p>0.05). Conclusion: The hyperglycemia, high insulin, and protracted glucose and insulin curves, the initial decrease in the insulin/glucose ratio indicates that there was an unexpected glucose tolerance to acute intravenous glucose loading in water buffalo compared with other ruminants. The possibly suggested intravenous glucose load in buffaloes is about 5.09–8.28 mmol/l.

Pancreatic endocrine responses to substance P and calcitonin gene-related peptide in conscious calves.

Both substance P (SP) and calcitonin gene-related peptide (CGRP; 0.13 micrograms.min-1.kg-1 for 10 min) produced a significant rise in arterial plasma pancreatic polypeptide (PP) concentration, and additive responses were obtained when both peptides were infused simultaneously and/or with acetylcholine (0.7 micrograms.min-1.kg-1 ia). The PP response to SP was abolished by intravenous infusions of glucose, whereas those to CGRP and acetylcholine were not significantly affected. Neither SP nor CGRP had any effect on plasma insulin concentration, either in the presence or absence of exogenous glucose, whether infused singly or together, or in the presence of acetylcholine. SP, but not CGRP, produced a small but statistically significant rise in mean plasma glucagon concentration when infused together with acetylcholine. These results suggest that SP and CGRP may modulate the secretion of PP and glucagon in the normal conscious calf but not that of insulin. It is also possible that SP modulates secretion of pancreatic glucagon in these animals.

Plasma glucose thresholds for counterregulation after an oral glucose load

Glucose counterregulation (GCR) plays an important role in the transition between exogenous and endogenous glucose delivery after an oral glucose load. This response is initiated when plasma glucose concentrations are decreased below threshold levels, previously defined in studies of insulin-induced hypoglycemia. In this study, we tested the plasma glucose thresholds for activation of the GCR response under more physiologic circumstances, ie, after glucose ingestion. We studied 20 normal subjects for 300 minutes after 75 g of oral glucose. Between 150 and 300 minutes, blood samples and symptom scores were obtained at 10-minute intervals. After oral glucose, individual glucose nadirs were observed over a wide time range (160 to 290 minutes). Mean glucose concentrations decreased from 5.3 ± 0.2 mmol/L at 30 minutes before the nadir (−30 minutes) to 3.8 ± 0.2 mmol/L at the nadir (0 minutes). Mean plasma epinephrine concentrations increased from 210 ± 35 pmol/L, were significantly elevated at −10 minutes ( P < .05), and peaked at +20 minutes (1,008 ± 184 pmol/L, P < .001). Mean plasma glucagon concentrations were significantly increased over baseline (100%) at +10 minutes ( P < .001) and peaked at +30 minutes (122% ± 7%, P < .001). Seven subjects (out of 15 tested) developed symptoms. Quantitative evaluation revealed a peak in the mean symptom score at +20 minutes, an increase from 0.4 ± 0.3 to 2.6 ± 0.1 arbitrary units ( P < .06). Plasma glucose thresholds for epinephrine, glucagon, and appearance of symptoms were estimated to be 4.2 ± 0.2, 3.8 ± 0.2, and between 2.9 and 3.3 mmol/L, respectively, similar to those found during studies of insulin-induced hypoglycemia. We conclude that the levels and hierarchy of plasma glucose thresholds for GCR are maintained during the late phase after an oral glucose load. Also, even in normal subjects, mild symptoms may occur and peak together with epinephrine after the gluose nadir.

The role of the sympathetic system in the control of insulin release in response to hyperglycaemia in conscious calves.

The effects of the adrenoceptor blocking agents, phentolamine and propranolol, on the release of pancreatic glucagon and insulin in response to exogenous glucose have been investigated in conscious 2--6-week-old calves. There were no significant differences between the changes in mean plasma glucagon or insulin concentration, which occurred in response to hyperglycaemia, in calves pre-treated with both propranolol and phentolamine, phentolamine alone and normal calves. However, the rise in mean plasma insulin concentration was effectively abolished by pre-treatment with propranolol alone and there was a small but significant fall in mean plasma glucagon concentration which was not observed in any of the other groups. The results are discussed in relation to previous studies of the role of the autonomic innervation to the endocrine pancreas in the control of insulin release during hyperglycaemia in conscious calves and weaned lambs.

Effects of certain metabolites on pancreatic endocrine responses to gastrin-releasing peptide in conscious calves.

The effects of intravenous infusions of synthetic gastrin-releasing peptide (GRP; 5 pmol/kg X min) have been investigated in 3- to 6-week-old conscious calves receiving continuous intravenous infusions of either glucose or amino acids or both at a dose of 0.03 mmol/kg X min and the results compared with the effects of the same dose of the peptide in control calves. Pre-treatment with amino acids alone caused a statistically significant fall in mean plasma glucose concentration, which was associated with a significant rise in mean pancreatic glucagon concentration. Additional infusion of glucose prevented this rise in plasma glucose concentration and resulted in a delayed, but very substantial rise in mean plasma insulin concentration. Pre-treatment with amino acids alone substantially and significantly increased the rise in mean plasma insulin that occurred in response to GRP. The rise in mean plasma glucagon concentration in response to GRP that occurred in the control group, the group pre-treated with amino acids alone and the group given both glucose and amino acids, was virtually eliminated in the group pre-treated with glucose alone. The normal rise in plasma pancreatic polypeptide concentration in response to GRP was invariably abolished in the presence of amino acids. No significant change in either mean neurotensin-like or gastric-inhibitory-peptide-like immunoreactivity was observed in response to GRP in any of these groups. The results are discussed in relation to possible physiological functions that GRP may subserve.

The relation between catecholamines, glucagon and pancreatic polypeptide during hypoglycaemia in man

The effects of insulin hypoglycaemia (0.15 IU/kg) on plasma adrenaline, noradrenaline, dopamine, glucagon and pancreatic polypeptide (PP) concentrations were investigated in 6 adrenalectomized subjects and 6 healthy controls. Both the rise in mean plasma insulin and the fall in mean blood glucose concentration were closely similar in the two groups. Mean plasma adrenaline concentration rose by about 3 nmol/l in the normal subjects, but remained unchanged in adrenalectomized subjects. Mean plasma noradrenaline concentration increased by about 2 nmol/l in both groups. Despite the large difference in adrenaline concentrations during hypoglycaemia, there was no significant difference between the responses of the endocrine pancreas of the normal and adrenalectomized subjects. Thus, mean plasma glucagon concentration rose by about 30 pmol/l and mean plasma PP concentration by about 150 pmol/l in each group. We conclude that the release of glucagon and PP during hypoglycaemia does not depend upon changes in plasma adrenaline concentration in man.

The effect of glucagon infusion on kidney function in short-term insulin-dependent juvenile diabetics.

Kidney function was studied in nine, metabolically well controlled, short-term insulin-dependent male diabetics before and during glucagon infusion of 4 to 5 and 8 to 10 ng/kg/min. Glomerular filtration rate, effective renal plasma flow (steady-state infusion technique, with urinary collections, using 125I-iothalamate and 131I-iodohippurate), and urinary albumin and beta 2-microglobulin excretion rates were measured. The mean plasma glucagon concentration increased during infusion from 254 +/- 19 pg/ml to 440 +/- 31 pg/ml (low dose) and 730 +/- 52 pg/ml (high dose). Glomerular filtration rate increased in all subjects from 133 +/- 5 before the glucagon infusion to 141 +/- 4 with the low dose, and 148 +/- 7 ml/min/1.73 m2 with the high dose (p < 0.01). The increase in glomerular filtration rate correlated with the rise in plasma glucagon concentration (r = 0.67; p < 0.01). Renal plasma flow increased from 530 +/- 21 before the glucagon infusion to 555 +/- 20 with the low dose and 572 +/- 29 ml/min/1.73 m2 with the high dose (p < 0.01). Urinary beta 2-microglobulin excretion rate rose from 5.8 +/- 1.0 before infusion to 8.7 +/- 1.7 with the low dose, and 17.9 +/- 5.7 micrograms X 10(-2)/min with the high dose (p < 0.01). Urinary albumin excretion remained unchanged during the glucagon infusion. These results suggest that glucagon may contribute to the reversible elevation of glomerular filtration rate typically found in poorly regulated insulin-dependent diabetics, but not to the moderate elevation found in well controlled diabetics.

Plasma glucagon concentrations in sheep: their regulation and relation to concentrations of insulin and growth hormone.

A radioimmunoassay for glucagon has been used to study the regulation of the plasma glucagon concentration in sheep. The mean plasma glucagon concentra� tion after an overnight fast was 0�20 ng/ml in crossbred sheep and 0 �12 ng/ml in Merinos. During a more prolonged fast plasma glucagon concentrations declined.