Epidermal growth factor excretion and receptor binding in diabetic rats

Hwang, David; Lev-Ran, Arye; Tay, Yee-Chaw; Chen, C.R.; Dev, Nirmitha

doi:10.1016/0024-3205(89)90265-8

Cited by 17 publications

(8 citation statements)

References 16 publications

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“…Epidemiological studies suggest that this may be a causative factor in the epidemic of diabetes seen in the United States and other Western countries. Studies in rats have shown that fructose feeding produces a moderate hypertension associated with glucose intolerance and dyslipidemia (10,24,26,33). Our group (15) reported that a high-fructose diet in C57BL mice increased blood pressure and plasma cholesterol.…”

Section: Discussionmentioning

confidence: 93%

Genetic and dietary interactions: role of angiotensin AT_1a receptors in response to a high-fructose diet

Farah

Elased²,

Morris³

2007

American Journal of Physiology-Heart and Circulatory Physiology

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The renin-angiotensin system (RAS) has been implicated in the cardiovascular complications of diabetes. We showed that a high-fructose diet increases blood pressure and plasma angiotensin and impairs glucose tolerance. We investigated the role of angiotensin AT(1a) receptors in the development of fructose-induced cardiovascular and metabolic dysfunction. Male angiotensin AT(1a) knockout (AT1aKO) and wild-type (AT1aWT) mice with arterial telemetric catheters were fed a standard diet or one containing 60% fructose. Fructose increased mean arterial pressure (MAP) in AT1aWT but only during the dark phase (8% increase). In AT1aKO mice, fructose unexpectedly decreased MAP, during both light and dark periods (24 and 13% decrease, respectively). Analytical methods were used to measure systolic arterial pressure (SAP) and pulse interval (PI) variability in time and frequency domains. In fructose-fed AT1aWT mice, there was an increase in SAP variance and its low-frequency (LF) domain (11 +/- 3 vs. 23 +/- 4 mmHg(2), variance, and 7 +/- 2 vs. 17 +/- 3 mmHg(2), LF, control vs. fructose, P < 0.004). There were no changes in SAP variance in AT1aKO mice. Depressor responses to alpha(1)-adrenergic blockade were augmented in fructose-fed AT1a WT compared with AT1aKO mice. Fructose inhibited glucose tolerance with a greater effect in AT1aWT mice. Fructose increased plasma cholesterol in both groups (P < 0.01) and reduced ANG II in AT1aKO mice. Results document prominent interactions between genetics and diet with data showing that in the absence of angiotensin AT(1a) receptors, a fructose diet decreased blood pressure.

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Section: Discussionmentioning

confidence: 93%

Genetic and dietary interactions: role of angiotensin AT_1a receptors in response to a high-fructose diet

Farah

Elased²,

Morris³

2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…Although recently Hwang et al [45] found that EGF in the submandibular gland and urine increased in diabetic rats and decreased in insulin-treated rats, they did not study the role of EGF in renal hypertrophy in diabetic rats.…”

Section: Discussionmentioning

confidence: 99%

Epidermal Growth Factor in Renal Hypertrophy in Streptozotocin-Diabetic Rats

Guh¹,

Lai²,

Shin³

et al. 1991

Nephron

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Epidermal growth factor (EGF) concentrations in the plasma, kidneys and urine of 31 streptozotocin-diabetic rats and 21 insulin-treated diabetic rats were measured to study the role of EGF in initiating renal hypertrophy in the diabetic rats. Renal hypertrophy occurred from day 7 in the diabetic rats, but not in the insulin-treated rats. Renal EGF was not different between the diabetic and control rats, while that in the insulin-treated rats was significantly less than in the diabetic rats. There were no significant changes in plasma EGF in any of the rats. Urine EGF was 119 ± 7.9 ng/day at day 7 in the control rats but it was significantly increased from day 2 in the diabetic rats (320 ± 52.9 ng/day at day 2 and 298 ± 18.4 ng/day at day 7), while in the insulin-treated rats it was significantly less than that in the diabetic rats (134 ± 8.34 ng/day at day 2 and 220 ± 15.2 ng/day at day 7). Since the kidney is the main source of urine EGF and EGF has been shown to induce renal growth both in vitro and in vivo, we conclude that EGF may have initiated renal hypertrophy in diabetic rats.

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“…In rats with spontaneous or chemically induced diabetes urinary EGF excretion is increased. 233 In diabetic mice with early STZ-induced diabetes and also in ob/ob mice with chronic diabetes, urine EGF excretion is increased.232 This differerxe from humans may reflect species differences or the lack of kidney disease in the anim-als at the time of study.…”

Section: Epidermal Growth Factor (Egf)mentioning

confidence: 97%

Renal Hypertrophy and Kidney Disease in Diabetes

Rabkin

Fervenza

1996

Diabetes Metab. Rev.

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Epidermal growth factor excretion and receptor binding in diabetic rats

Cited by 17 publications

References 16 publications

Genetic and dietary interactions: role of angiotensin AT_1a receptors in response to a high-fructose diet

Genetic and dietary interactions: role of angiotensin AT_1a receptors in response to a high-fructose diet

Epidermal Growth Factor in Renal Hypertrophy in Streptozotocin-Diabetic Rats

Renal Hypertrophy and Kidney Disease in Diabetes

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Epidermal growth factor excretion and receptor binding in diabetic rats

Cited by 17 publications

References 16 publications

Genetic and dietary interactions: role of angiotensin AT1a receptors in response to a high-fructose diet

Genetic and dietary interactions: role of angiotensin AT1a receptors in response to a high-fructose diet

Epidermal Growth Factor in Renal Hypertrophy in Streptozotocin-Diabetic Rats

Renal Hypertrophy and Kidney Disease in Diabetes

Contact Info

Product

Resources

About

Genetic and dietary interactions: role of angiotensin AT_1a receptors in response to a high-fructose diet

Genetic and dietary interactions: role of angiotensin AT_1a receptors in response to a high-fructose diet