Early insulin response after food intake in geese

1992 ◽  
Vol 263 (4) ◽  
pp. R782-R784
Author(s):  
H. Karmann ◽  
N. Rideau ◽  
T. Zorn ◽  
A. Malan ◽  
Y. Le Maho

Plasma glucose and insulin levels were measured in chronically catheterized, freely moving, undisturbed geese, which were offered a free standard meal after an overnight fast. The insulin level markedly rose within the first minute after the start of food ingestion, whereas plasma glucose did not increase. This early insulin response was not correlated with the size of the meal. In contrast, both postabsorptive insulin response and plasma glucose changes were dependent on meal size. When a small amount of food (2-6 g) was eaten, insulin returned to basal level within 30 min, whereas plasma glucose remained unchanged. Larger meals (15-20 g) maintained plasma insulin at a higher level and induced a sustained rise of plasma glucose. These results indicate that there is a cephalic phase of insulin secretion at the beginning of the meal in birds as previously described in mammals.

1978 ◽  
Vol 235 (5) ◽  
pp. E467 ◽  
Author(s):  
A F Philipps ◽  
B S Carson ◽  
G Meschia ◽  
F C Battaglia

The relationships between arterial plasma insulin, glucose, and fructose concentrations during the fed and fasted state were studied in seven fetal lambs and their mothers. A significant correlation between insulin and glucose concentration was noted in all fetal lambs and in their mothers. Fetal sensitivity to glucose, as measured by the slopes of the insulin-response curves, was equal to that of the adult although the fetal response was shifted to the left of the maternal. Glucose infusion in four fetal lambs caused significant insulin elevations but no early insulin response (phase I). Maternal fasting caused no alteration in glucose-induced response in the fetus. Similar glucose infusions in newborn and 1-mo-old lambs demonstrated significant early-phase insulin secretion. Basal insulin to glucose ratios were consistent with an adult pattern as early as 3 days after birth.


1975 ◽  
Vol 229 (4) ◽  
pp. 1019-1022 ◽  
Author(s):  
JH Strubbe ◽  
AB Steffens

Blood glucose and insulin levels were measured in undisturbed and free-moving rats. The insulin level rises already in the 1st min after the start of food ingestion, whereas the glucose level begins to increase only in the 3rd min if carbohydrate-rich food is eaten. This early rise in insulin level is observed also under conditions in which either carbohydrate-free food or even "food" without any caloric value is offered. The smell of food cannot produce this early insulin response. It is concluded that in the rat other factors besides a rise in nutrient content in the blood produce insulin release in the first minutes after food ingestion.


1991 ◽  
Vol 261 (4) ◽  
pp. E430-E436 ◽  
Author(s):  
K. L. Teff ◽  
R. D. Mattes ◽  
K. Engelman

The existence and reliability of cephalic phase insulin release (CPIR) were tested in 20 normal weight males. Each subject was challenged three times with the same food stimulus over a 5-day period. Four baseline blood samples were taken at 5-min intervals before food ingestion and then every 2 min for 16 min postingestion. Significant increases in plasma insulin were found at 4 min postingestion on each trial day. CPIR was found to be highly reproducible between trials (r = 0.83; P less than 0.001). Fifty percent of the subjects exhibited a significant increase of plasma insulin above their own baseline mean on the first trial, whereas 75 and 72% exhibited increases on trials 2 and 3, respectively. Only two subjects (10%) did not demonstrate a response on any trial. A significant decline in plasma glucose was observed at 4 min postingestion on trials 2 and 3. No significant changes in plasma glucagon were found during any trial day. This study confirms a reliable CPIR in normal weight males.


PEDIATRICS ◽  
1981 ◽  
Vol 67 (4) ◽  
pp. 498-501
Author(s):  
Robert Cicco ◽  
Ian R. Holzman ◽  
David R. Brown ◽  
Dorothy J. Becker

Some formulas designed for premature infants contain glucose polymer (GP) as part of their carbohydrate content. GP tolerance tests and lactose tolerance tests were performed on 11 healthy premature infants at 2 to 3 weeks of age to compare their ability to digest and absorb GP and lactose. Total plasma reducing substances (TPRS), plasma insulin (PI), and plasma glucose were measured 10 minutes before and 30, 60, and 120 minutes after the oral carbohydrate test meal. Lactose and GP stimulated a significant increase in TPRS at 30 and 60 minutes and produced similar glycemic responses. However, GP stimulated a smaller PI response whether measured as the area under the PI response curve or as the PI/TPRS ratio. It was concluded that although GP and lactose evoke similar glycemic responses, they differ in their abilities to stimulate insulin secretion. The mechanism controlling this differential insulin response is unknown.


1992 ◽  
Vol 263 (3) ◽  
pp. R615-R618 ◽  
Author(s):  
J. H. Strubbe

Blood glucose and plasma insulin concentrations were measured in blood sampled via a cardiac catheter in freely moving rats. To obtain a rapid conditioned cephalic phase of insulin secretion, rats were habituated to one of two feeding schedules. Clock-activated opening of doors in front of the food hopper imposed a feeding schedule of either six meals per day or two meals per day. When the doors were opened in both conditions, insulin increased rapidly during the first minute of feeding in the middle of the light phase. However, when presented an empty food hopper immediately after door opening, only rats in the two meal per day condition showed raised insulin levels and not rats in the six meal per day condition. This response was abolished following pharmacological blockade of nicotinic receptors with hexamethonium and muscarinic receptors with atropine. The present study shows that rapid conditioned insulin secretion can be evoked within one minute by a meal-associated stimulus. These results further indicate that this conditioned insulin secretion is vagally mediated and that its occurrence is dependent on the nature of the feeding schedule.


1988 ◽  
Vol 255 (6) ◽  
pp. R1035-R1040
Author(s):  
R. Hoo-Paris ◽  
M. L. Jourdan ◽  
L. C. Wang ◽  
R. Rajotte

In hypothermia, impairment of metabolic substrate mobilization and utilization may be a factor limiting survival. By use of a newly developed technique, substrate profiles and their regulation by insulin were examined in hypothermic rats (body temperature 19 degrees C) over 24 h. Plasma glucose concentrations increased to approximately 300 mg/dl during cooling and remained high throughout the period of hypothermia. Free fatty acid (FFA) concentration was not altered during cooling or during the first 10 h of hypothermia (approximately 700 mu eq/l) but progressively decreased thereafter, reaching 420 mu eq/l by 20 h. Plasma insulin decreased dramatically during cooling and remained very low (9 +/- 2 microU/ml) during the whole period of hypothermia, reflecting the suppression of insulin secretion by isolated islets at low temperatures. To test he hypothesis that suppression of endogenous insulin secretion may hamper glucose utilization and thus limit survival in hypothermia, exogenous insulin was administered. At doses of 0.1, 0.5, and 1 U/kg intravenously, insulin slowly decreased plasma glucose and FFA. However, at 0.1 and 1 U/kg intraperitoneally, insulin resulted in a dose-dependent decrease in survival time in the hypothermic rat. It is possible that the antilipolytic effect of insulin may have outweighed any beneficial effect of improving glucose utilization in hypothermia.


2003 ◽  
pp. 403-406 ◽  
Author(s):  
L Briatore ◽  
G Andraghetti ◽  
R Cordera

OBJECTIVE: The independent role of glucose and insulin in ghrelin regulation is still controversial; this is also because in healthy subjects it is difficult to isolate the increase of glucose from that of insulin. The aim of this study was to discriminate the effect of glucose increase alone and early insulin response on plasma ghrelin, comparing ghrelin variation after i.v. glucose between healthy subjects and type 2 diabetic (T2DM) subjects, in whom the early insulin response to i.v. glucose is abolished. METHODS: Plasma glucose, insulin and ghrelin levels were measured 0, 3, 5, 10, 30, 45 and 60 min after a 5 g glucose i.v. bolus in seven healthy control subjects and eight T2DM subjects. RESULTS: There were no significant differences in body mass index, basal insulin and basal ghrelin between T2DM and healthy subjects. Basal glucose levels were higher in T2DM subjects than in controls. After i.v. glucose administration, plasma glucose increased significantly in both groups and the glucose peak was higher in T2DM subjects than in controls (9.67+/-1.25 (s.d.) vs 6.88+/-1.00 mmol/l, P<0.01). Insulin increased rapidly in controls, while in T2DM subjects, plasma insulin did not rise in the first 10 min. After the glucose bolus, plasma ghrelin showed a significant reduction both in controls and in T2DM subjects after 5 min. CONCLUSION: These findings indicate that a low-dose i.v. glucose bolus reduces ghrelin both in controls and in T2DM subjects and therefore that early insulin response does not affect plasma ghrelin.


2000 ◽  
Vol 278 (6) ◽  
pp. E1097-E1103 ◽  
Author(s):  
Carmen Alvarez ◽  
Danielle Bailbe ◽  
Françoise Picarel-Blanchot ◽  
Eric Bertin ◽  
Ana-Maria Pascual-Leone ◽  
...  

The availability of the Goto-Kakisaki (GK) rat model of non-insulin-dependent diabetes mellitus prompted us to test the effect of a limited period of undernutrition in previously diabetic young rats on their insulin secretion and insulin action during adult age. Four-week-old female GK rats were either food restricted (35% restriction, 15% protein diet) or protein and energy restricted (35% restriction, 5% protein diet) for 4 wk. Food restriction in the young GK rat lowered weight gain but did not aggravate basal hyperglycemia or glucose intolerance, despite a decrease in basal plasma insulin level. Furthermore, the insulin-mediated glucose uptake by peripheral tissues in the GK rat was clearly improved. We also found that food restriction, when it is coupled to overt protein deficiency in the young GK rat, altered weight gain more severely and slightly decreased basal hyperglycemia but conversely aggravated glucose tolerance. Improvement of basal hyperglycemia was related to repression of basal hepatic glucose hyperproduction, despite profound attenuation of basal plasma insulin level. Deterioration of tolerance to glucose was related to severe blunting of the residual glucose-induced insulin secretion. It is, however, likely that the important enhancement of the insulin-mediated glucose uptake helped to limit the deterioration of glucose tolerance.


2000 ◽  
Vol 279 (6) ◽  
pp. R2179-R2188 ◽  
Author(s):  
Benjamin T. Jackson ◽  
George J. Piasecki ◽  
Herbert E. Cohn ◽  
Wayne R. Cohen

In this study, we investigated the way in which fetal insulin secretion is influenced by interrelated changes in blood glucose and sympathoadrenal activity. Experiments were conducted in late gestation sheep fetuses prepared with chronic peripheral and adrenal catheters. The fetus mounted a brisk insulin response to hyperglycemia but with only a minimal change in the glucose-to-insulin ratio, indicating a tight coupling between insulin secretion and plasma glucose. In well-oxygenated fetuses, α2-adrenergic blockade by idazoxan effected no change in fetal insulin concentration, indicating the absence of a resting sympathetic inhibitory tone for insulin secretion. With hypoxia, fetal norepinephrine (NE) and epinephrine secretion and plasma NE increased markedly; fetal insulin secretion decreased strikingly with the degree of change related to extant plasma glucose concentration. Idazoxan blocked this effect showing the hypoxic inhibition of insulin secretion to be mediated by a specific α2-adrenergic mechanism. α2-Blockade in the presence of sympathetic activation secondary to hypoxic stress also revealed the presence of a potent β-adrenergic stimulatory effect for insulin secretion. However, based on an analysis of data at the completion of the study, this β-stimulatory mechanism was seen to be absent in all six fetuses that had been subjected to a prior experimentally induced hypoxic stress but in only one of nine fetuses not subjected to this perturbation. We speculate that severe hypoxic stress in the fetus may, at least in the short term, have a residual effect in suppressing the β-adrenergic stimulatory mechanism for insulin secretion.


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