scholarly journals The intravenous glucose tolerance and postprandial glucose tests may present different responses in the evaluation of obese dogs

2011 ◽  
Vol 106 (S1) ◽  
pp. S194-S197 ◽  
Author(s):  
Márcio Antonio Brunetto ◽  
Fabiano César Sá ◽  
Sandra Prudente Nogueira ◽  
Márcia de Oliveira Sampaio Gomes ◽  
Amanda Gullo Pinarel ◽  
...  

The present study compared the intravenous glucose tolerance test (IVGTT) and the glucose postprandial response (GPPR) test for the evaluation of glucose metabolism in obese dogs. A total of ten owned obese dogs (body condition score (BCS) of 9; fat mass, 45·7 (sem 1·51) %) were used. These dogs had their weight reduced by 20 % (BCS, 8; fat mass, 33·5 (sem 1·92) %; P < 0·001), designated as weight-reduced (WR) group. A control group of ten Beagle dogs was also included (BCS, 4·5; fat mass, 18·3 (sem 1·38) %; P < 0·01). Glucose tolerance was measured by two methods: IVGTT (infusion of 0·5 g of glucose/kg body weight) and GPPR (consumption of cooked rice to achieve 6 g of starch/kg body weight). When using the IVGTT, the area under the curve (AUC) for glucose and maximum glycaemia were higher for obese dogs compared with controls (P < 0·05), with intermediate results for the WR group (P>0·05). Basal insulin, insulin response peak, insulinogenic index and the AUC for insulin increment from 0 to 15 min and from 60 to 120 min were higher for the obese group (P < 0·05), while the WR group and control dogs showed similar results (P>0·05). When using the GPPR test, the AUC for insulin increment from 0 to 120 min was higher for the obese group compared with the control group (P < 0·05) and intermediate for the WR group (P>0·05). However, the AUC for insulin increment from 120 to 360 min was similar between the obese and WR groups (P>0·05), while it was lower for the control group (P < 0·05). The IVGTT showed that the loss of 20 % body weight resulted in an improvement of glucose control with reduced insulin secretion, and these same WR dogs showed higher insulin secretion with values similar to those of obese dogs when the GPPR test was used.

1995 ◽  
Vol 268 (2) ◽  
pp. R475-R479 ◽  
Author(s):  
B. Balkan ◽  
B. E. Dunning

Prolonged hyperglycemia impairs the in vitro insulin release by islets of Langerhans in response to glucose but exaggerates the in vivo insulin response. We hypothesized that this discrepancy results from increased vagal stimulation of the islets. Conscious chronically cannulated rats were infused with glucose (15 mg/min) or saline for 48 h. Three hours thereafter, an intravenous glucose tolerance test was performed with or without prior injection of atropine (0.2 mg). Atropine markedly (> 70%) reduced the insulin response in glucose-infused, but not in saline-infused, rats. Glucose-infused rats displayed basal hypoglycemia but normal glucose excursions during an intravenous glucose tolerance test. It is concluded that prolonged hyperglycemia produces exaggerated muscarinic activation of the beta-cells that will persist > or = 3 h after the termination of the glucose infusion and normalizes in vivo insulin secretion. It is possible that increased parasympathetic activation of the pancreas might constitute a general mechanism to maintain insulin output when the demand for insulin exceeds the inherent beta-cell responsiveness.


1983 ◽  
Vol 245 (6) ◽  
pp. E575-E581 ◽  
Author(s):  
A. L. Vallerand ◽  
J. Lupien ◽  
L. J. Bukowiecki

The metabolic interactions of cold exposure, cold acclimation, and starvation on glucose tolerance and plasma insulin levels were studied in precannulated, unrestrained, and unanesthetized rats. Cold exposure (48 h at 5 degrees C) significantly reduced the insulin response to intravenous glucose injection (P less than 0.01) while improving glucose tolerance (P less than 0.01). Starvation (48 h at 25 degrees C) also reduced the insulin response (P less than 0.01) but did not significantly alter glucose tolerance. “Accelerated starvation” induced by starving rats for 48 h at 5 degrees C dramatically reduced both basal and glucose-stimulated insulin levels while even improving glucose tolerance, resulting in a 15-fold reduction in the insulinogenic index. Cold acclimation (3 wk at 5 degrees C) induced essentially the same alterations as cold exposure. Approximately reversed changes were observed when cold-acclimated rats were returned to a warm environment for 15–18 h. Results from these studies indicate that 1) cold exposure and starvation, but not cold acclimation, act synergistically in decreasing the sensitivity and/or the capacity of pancreatic islets for secreting insulin in response to glucose stimulation; 2) glucose tolerance and possibly insulin sensitivity of peripheral tissues are enhanced by cold exposure and starvation, although glucose tolerance is improved by cold exposure only, not by starvation; 3) an improved glucose tolerance with barely detectable plasma insulin levels was obtained in cold-starved rats under normal physiological conditions.


1999 ◽  
Vol 276 (4) ◽  
pp. E739-E746 ◽  
Author(s):  
M. Dawn McArthur ◽  
Dan You ◽  
Kim Klapstein ◽  
Diane T. Finegood

To determine the importance of insulin for glucose disposal during an intravenous glucose tolerance test in rats, experiments were performed in four cohorts of conscious unrestrained rats fasted overnight. In cohorts 1- 3, a bolus of tracer ([3-3H]glucose, 50 μCi) was given alone, with glucose (0.3 g/kg) to induce an endogenous insulin response (∼1,100 pmol/l), or with exogenous insulin to give physiological (1,700 pmol/l) or supraphysiological (12,000 pmol/l) plasma levels. Raising plasma insulin within the physiological range had no effect ( P > 0.05), but supraphysiological levels induced hypoglycemia (7.3 ± 0.2 to 3.6 ± 0.2 mmol/l) and increased [3H]glucose disappearance rate ( P < 0.001). In cohort 4, a primed, continuous tracer infusion was started 120 min before saline or glucose bolus injection. [3H]glucose levels fell 15–20%, and the disappearance rate rose 36% ( P < 0.05) after glucose injection. These results indicate that in fasted rats a tracer bolus injection protocol is not sufficiently sensitive to measure the physiological effect of insulin released in response to a bolus of glucose because this effect of insulin is small. Glucose itself is the predominant mediator of glucose disposal after a bolus of glucose in the fasted rat.


1994 ◽  
Vol 267 (4) ◽  
pp. R1071-R1077 ◽  
Author(s):  
S. Karlsson ◽  
A. J. Scheurink ◽  
A. B. Steffens ◽  
B. Ahren

The impact of sensory nerves in glucose-stimulated insulin secretion and glucose tolerance was investigated in conscious mice treated neonatally with either capsaicin (Cap) or vehicle (Veh). At 10-12 wk after Cap, both the early (1 min) insulin secretory response to intravenous glucose (2.8 mmol/kg) (by 67%) and glucose elimination were potentiated (P < 0.05). In contrast, basal insulin, glucagon, and glucose were not affected by Cap. Plasma norepinephrine and epinephrine levels did not differ between Cap- and Veh-treated animals, whereas the increase in plasma insulin levels normally induced by alpha-adrenoceptor blockade by phentolamine was absent after Cap treatment. In isolated islets, the insulin secretory response to glucose (20 mmol/l), carbachol (0.1 mmol/l), or phentolamine (0.5 mmol/l) was not affected after Cap. It is concluded that sensory denervation by Cap results in increased glucose tolerance, which is in part because of a potentiated early insulin response to glucose. This potentiation does not seem secondary to altered plasma catecholamine levels or to altered islet secretory capacity. The results suggest rather that Cap-sensitive nerves, by a local effector function and/or as the afferent loop of a neural reflex, exert inhibitory influences on insulin secretion.


2021 ◽  
Vol 8 ◽  
Author(s):  
Kiriko Watanabe ◽  
Moritake Higa ◽  
Yoshimasa Hasegawa ◽  
Akihiro Kudo ◽  
Richard C. Allsopp ◽  
...  

Purpose: Regional differences in dietary patterns in Asian countries might affect the balance of insulin response and sensitivity. However, this notion is yet to be validated. To clarify the regional differences in the insulin response and sensitivity and their relationship to nutrients, we compared the insulin secretory response during an oral glucose tolerance test in Japanese participants.Methods: This observational retrospective cohort study analyzed the data from participants with normal glucose tolerance (NGT) from four distinct areas of Japan with regard to the food environment: Fukushima, Nagano, Tokushima, and Okinawa based on data available in the Japanese National Health Insurance database.Results: Although the glucose levels were comparable among the four regions, the insulin responses were significantly different among the regions. This difference was observed even within the same BMI category. The plot between the insulin sensitivity index (Matsuda index) and insulinAUC/glucoseAUC or the insulinogenic index showed hyperbolic relationships with variations in regions. The indices of insulin secretion correlated positively with fat intake and negatively with the intake of fish, carbohydrate calories, and dietary fiber.Conclusions: We found that significant regional differences in insulin response and insulin sensitivity in Japanese participants and that nutritional factors may be linked to these differences independently of body size/adiposity. Insulin response and insulin sensitivity can vary among adult individuals, even within the same race and the same country, and are likely affected by environmental/lifestyle factors as well as genetic traits.


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