Intravenous glucose tolerance test—derived glucose effectiveness in endurance-trained rats

Tokuyama, Kumpei; Suzuki, Masashige

doi:10.1016/s0026-0495(98)90219-0

Cited by 15 publications

(15 citation statements)

References 37 publications

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“…In addition, when the data were analyzed by Pacini and Bergman's minimal model (30), which has been validated in rodents (27,28,31,40), the three EtOH groups of rats had a decreased S I . There was a hyperbolic relationship between AIR and S I , indicating that insulin resistance was associated with a compensatory increase in insulin secretion (7,18).…”

Section: Discussionmentioning

confidence: 99%

“…Blood (0.1 ml) was subsequently drawn 1, 2, 3, 5, and 8 min after glucose injection. Regular insulin (Humulin, 0.1 U/kg; Eli Lilly, Indianapolis, IN) was then injected through the femoral vein, and blood collection continued at 10,12,14,16,18,20,22,25,30,40,60, and 90 min. The withdrawn volume was replaced with normal saline.…”

Section: Animalsmentioning

confidence: 99%

“…The units of K G are percent per minute (1). Insulin sensitivity index (SI) was determined by minimal modeling (27,28,31,40) by using Pacini and Bergman's MINMOD program (30). Products of S I with AIR were used as the disposition index (DI), which has been proposed in dogs (7), humans (18), and mice (31) as representing insulin effect.…”

Section: Animalsmentioning

confidence: 99%

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Whole body insulin resistance in rat offspring of mothers consuming alcohol during pregnancy or lactation: comparing prenatal and postnatal exposure

Chen

Nyomba

2004

Journal of Applied Physiology

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This study examined the effects of maternal ethanol (EtOH) consumption during pregnancy or lactation on glucose homeostasis in the adult rat offspring. Glucose disposal was determined by minimal model during an intravenous glucose tolerance test in rats that had a small or normal birth weight after EtOH exposure in utero and in rats whose mothers were given EtOH during lactation only. All three EtOH groups had decreased glucose tolerance index and insulin sensitivity index, but their glucose effectiveness was not different from that of controls. In addition, EtOH rat offspring that were small at birth had elevated plasma, liver, and muscle triglyceride levels. The data show that EtOH exposure during pregnancy programs the body to insulin resistance later in life, regardless of birth weight, but that this effect also results in dyslipidemia in growth-restricted rats. In addition, insulin resistance is also evident after EtOH exposure during lactation.

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Section: Discussionmentioning

confidence: 99%

Section: Animalsmentioning

confidence: 99%

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Whole body insulin resistance in rat offspring of mothers consuming alcohol during pregnancy or lactation: comparing prenatal and postnatal exposure

Chen

Nyomba

2004

Journal of Applied Physiology

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“…Changes in insulin sensitivity after endurance training are well documented in muscle and adipose tissue, both in humans and in animals (Borghouts and Keizer, 2000;Dela et al, 1992;Devlin, 1992;Goodyear and Kahn, 1998;Ivy, 1996;James et al, 1984;Koivisto et al, 1986;Perron et al, 1986;Rodnick et al, 1987;Stallknecht et al, 2000;Suda et al, 1993;Tan and Bonen, 1987;Tokuyama and Suzuki, 1998). In contrast, as far as we know there are few studies concerning liver sensitivity to insulin.…”

Section: Hormonal Regulation Paradoxmentioning

confidence: 99%

Glucagon Receptors: Effect of Exercise and Fasting

Lavoie

2005

Can. J. Appl. Physiol.

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One paradox of hormonal regulation during exercise is the maintenance of glucose homeostasis after endurance training despite a lower increase in plasma glucagon. One explanation could be that liver sensitivity to glucagon is increased by endurance training. Glucagon exerts its effect through a 62 KDa glycoprotein receptor, member of the G protein-coupled receptor. To determine whether changes with exercise in glucagon sensitivity occurred at the level of the glucagon receptor (GR), binding characteristics of hepatic glucagon receptors were ascertained in rat purified plasma membranes. Saturation kinetics indicated no difference in the dissociation constant or affinity of glucagon receptor, but a significantly higher glucagon receptor binding density in liver in endurance trained compared to untrained animals. Along with endurance training, it appears that fasting also changes GR binding characteristics. In animals fasting 24 hrs, a significant increase in glucagon receptor density was also reported. Although the exact mechanism remains unknown, there is no doubt that the liver can adapt to physiological stress through modulation of GR binding characteristics to enhance the hepatic glucose production responsiveness to glucagon.

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“…glucose load was evaluated using the glucose disappearance constant (KG) calculated as the slope of the least-square regression line relating the natural logarithm of the glucose concentration to time between 5 and 15 min, expressed as %/min (11). For the insulin responses to the i.v.…”

Section: Parameters and Statisticsmentioning

confidence: 99%

Progesterone stimulates pancreatic cell proliferation in vivo

Nieuwenhuizen

Schuiling²,

Liem³

et al. 1999

European Journal of Endocrinology

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Treatment of cyclic and pregnant rats with progesterone stimulates cell proliferation within the islets of Langerhans. It was investigated whether this effect of progesterone depends on sex and/or the presence of the gonads or the presence of oestradiol. For this purpose, Silastic tubes containing progesterone were inserted s.c. in intact and gonadectomized male and female rats, and in gonadectomized female rats treated with oestradiol. After 6 days of progesterone treatment, rats were infused for 24 h with 5-bromo-2 0 -deoxyuridine (BrdU) and dividing cells were identified in pancreatic sections by immunostaining for BrdU. Progesterone treatment increased islet-cell proliferation in intact male and female rats (P<0.05), but not in gonadectomized male and female rats or in gonadectomized female rats supplemented with oestradiol. Furthermore, in intact male and female rats, progesterone treatment also stimulated cell proliferation in extra-islet pancreatic tissue (P<0.05). Identification of the proliferating cells, by double-immunocytochemistry, revealed that progesterone treatment stimulated proliferation of both a and b cells within the pancreatic islets. In extra-islet pancreatic tissue, progesterone treatment stimulated proliferation in both duct (cytokeratin 20-immunoreactive) and non-duct cells. Progesterone treatment did not increase the number of single glucagon or insulincontaining cells outside the pancreatic islets, nor that of cytokeratin 20/insulin double-positive cells, suggesting that progesterone treatment did not stimulate differentiation of duct cells into endocrine cells. Progesterone treatment did not affect insulin responses to an i.v. glucose load (0.5 g/kg body weight). It is concluded that progesterone stimulates pancreatic cell proliferation indirectly; gonadal factor(s), not identical to oestradiol, is (are) probably involved.

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Intravenous glucose tolerance test—derived glucose effectiveness in endurance-trained rats

Cited by 15 publications

References 37 publications

Whole body insulin resistance in rat offspring of mothers consuming alcohol during pregnancy or lactation: comparing prenatal and postnatal exposure

Whole body insulin resistance in rat offspring of mothers consuming alcohol during pregnancy or lactation: comparing prenatal and postnatal exposure

Glucagon Receptors: Effect of Exercise and Fasting

Progesterone stimulates pancreatic cell proliferation in vivo

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