Wound healing in normal and diabetic Chinese hamsters

Weringer, Elora J.; Arquilla, Edward R.

doi:10.1007/bf00252688

Cited by 37 publications

(12 citation statements)

References 17 publications

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“…Specifically, leukocyte infiltration [28,29] and the inflammatory phase of wound healing are disturbed [28][29][30][31] leading to abnormal tissue repair in diabetics. In addition, some experiments have shown that factors in diabetic serum inhibit leukocyte chemotaxis in vivo [32] and collagen synthesis in vitro [33].…”

Section: Discussionmentioning

confidence: 99%

Effects of Hexose Sugars: Glucose, Fructose, Galactose and Mannose on Wound Healing in the Rat

Kössi¹,

Ekfors

Niinikoski³

et al. 1999

Eur Surg Res

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The effects of four hexose sugars (D-glucose, D-fructose, D-galactose, D-mannose) on the developing granulation tissue in rats were examined. Cylindrical hollow sponge implants were used as an inductive matrix for the growth of granulation tissue. In the test group, the implants were injected with 0.1 ml of solution containing the different hexoses in 0.01, 0.1 and 1 M concentrations daily for 7 days while the implants of the control groups were injected with 0.1 ml of phosphate-buffered saline solution only. Analyses of granulation tissue and wound fluid in the sponge implants were carried out 7 days after implantation. The results demonstrated that galactose caused a significant increase in the accumulation of granulation tissue as estimated by histological analyses, but no significant differences were observed in various chemical analyses. In striking contrast, statistically significant decreases were observed in the number of leukocytes in wound fluid, in the amount of DNA, RNA, collagen hydroxyproline, nitrogen, hexosamines and uronic acids in sponges treated with 0.1 or 1 M mannose, reflecting decreased granulation tissue formation. This effect was also observed in histological analyses of the specimens. There were no major changes in sponges treated with glucose or fructose. In summary, the findings of the present study demonstrate that galactose may enhance wound healing and mannose treatment inhibits the inflammatory reaction in wound healing and decreases granulation tissue formation in an experimental wound model.

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Section: Discussionmentioning

confidence: 99%

Effects of Hexose Sugars: Glucose, Fructose, Galactose and Mannose on Wound Healing in the Rat

Kössi¹,

Ekfors

Niinikoski³

et al. 1999

Eur Surg Res

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“…128 -129 Also, wound healing of diabetic Chinese hamsters was characterized by increased edema with delayed and reduced vascular and cellular infiltration in the early healing period. 130 Diabetic Chinese hamsters have also been reported to have significantly increased numbers of somatotrophs which could produce hormonal antagonists to insulin. 131…”

Section: Morphologic Changes and Complicationsmentioning

confidence: 99%

The Chinese Hamster as a Model for the Study of Diabetes Mellitus

Gerritsen¹

1982

Diabetes

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Selection for and against diabetes and subsequent inbreeding of Chinese hamsters started in 1963. Currently there are six inbred sublines that have greater than 85% incidence of glycosuria and two control inbred nondiabetic sublines that are essentially free of glycosuria. At birth, hamsters from inbred sublines are considered prediabetic. There is phenotypic variation between diabetic sublines. Onset time, incidence of ketonuria, blood glucose, plasma insulin, glucagon and glycohydrolase levels vary from subline to subline, but pancreatic insulin and glucagon levels are consistently low and high, respectively, in all diabetic sublines compared with nondiabetics. Experimental breeding data suggest a minimum of two homozygous recessive genes for diabetes. It is not known if the inbred lines are similar diabetic genotypes, but the probability is high that modifier background genes vary from subline to subline.Chinese hamsters have diabetes ranging from mild to severe. Animals weighing 25 g can excrete up to 75 ml of urine containing 3 g of glucose per day. Fasting blood glucose as high as 500 mg/dl and 10 /nmol/ml of beta-hydroxybutyrate have been reported. Gluconeogenesis is elevated, and some glycolytic enzymes are decreased in severe diabetes. Low levels of renal acid glycohydrolase enzymes may contribute to glomerular capillary loop basement membrane thickening in diabetic hamsters. Caloric restriction per se or reduction of dietary fat prevented onset of hyperglycemia and hyperinsulinemia in prediabetics. Morphologic changes have been observed in pancreatic islets, kidney, nerve, blood vessels, eyes, brain, and genitourinary systems of diabetic Chinese hamsters. Pathogenesis of diabetes in this animal appears to be related to an increased demand for insulin. Initially there is a positive response to this demand by beta cells, but exhaustion occurs. This is followed by a decrease in beta-cell mass and relative or absolute insulin deficiency. DIABETES 37 (Suppl.

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“…On the basis of these studies, we suggest that the defect in cellular proliferation in diabetes mellitus is due to depletion of circulating growth factors other than insulin and somatomedins. (Endocrinology 112: 1026,1983) I NSULIN-deficient diabetes mellitus is characterized by growth retardation, weight loss, tissue atrophy, impaired wound healing, and impaired lymphocyte blast transformation (1)(2)(3). Similar features are seen in experimentally induced diabetes in the rodent (4)(5)(6).…”

mentioning

confidence: 92%

“…Proliferation of mesenchymal bone precursor cells has been shown to be impaired in streptozotocin-treated diabetic rats (12). Furthermore, fibroblast and vascular proliferation after dermal injury are reduced in spontaneously diabetic hamsters (3). These in vivo observations may result from the depletion of circulating growth factors necessary for cell proliferation, the presence of an inhibitor of cell division, or both in untreated diabetes.…”

mentioning

confidence: 97%

The Effect of Streptozotocin-Induced Diabetes Mellitus on the Ability of Rat Serum to Stimulate Human Fibroblast Proliferation

Murphy

Lazarus

1983

Endocrinology

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Impaired tissue repair, tumor growth, and diminished uterine response to /3-estradiol are characteristics of experimental diabetes mellitus; this may be due to a specific defect in cellular proliferation. The aim of this study was to determine whether circulating growth factors other than the somatomedins are deficient in diabetic rat serum. We examined the effect of streptozotocin-induced diabetes mellitus on the ability of rat serum to stimulate the growth of cultured human diploid skin fibroblasts, a cell line that has been shown to proliferate in somatomedin-depleted serum.Normal rat serum resulted in a dose-dependent increase in the number of human skin fibroblasts [HES; 2.78 ± 0.15 x 10 5 (±SEM) for 5% serum vs. 0.21 ± 0.02 X 10 s for no serum; P < 0.0005]. In contrast, serum from untreated diabetic rats resulted in significantly less proliferation than normal serum (0.35 ± 0.01 X 10 ft vs. 2.78 ± 0.15 x 10 5 ; P < 0.0005 for 5% diabetic and normal rat serum, respectively). Similarly, serum from untreated diabetic rats was significantly less potent in stimulating DNA synthesis (measured as tritiated thymidine incorporation into DNA) in quiescent growth-arrested fibroblasts (12,698 ± 612 vs. 7,242.8 ± 378.2 cpm/well; P < 0.0005 for 2.5% serum). Serum from insulin-treated diabetic rats was significantly more potent than serum from untreated diabetic rats in stimulating human skin fibroblast proliferation (1.66 ± 0.10 x 10 5 us. 0.39 ± 0.01 x 10 5 cells/well; P < 0.0005 for 2.5% serum) and DNA synthesis (11,475.6 ± 1,325.6 vs. 7,242 ± 378.2 cpm/well; P < 0.005 for 2.5% serum), but was not significantly different from normal rat serum despite the relatively poor metabolic control achieved with insulin treatment. Similar results were obtained when sera from untreated and insulin-treated diabetic rats were tested on other human fibroblast cell lines, including embryonic lung and adult skin fibroblasts. In some fibroblast cell lines, serum from insulin-treated diabetic rats was significantly less potent than normal rat serum.Impaired stimulation of fibroblast DNA synthesis by diabetic serum was not due to small molecules such as ketones, as dialyzed serum from untreated diabetic rats was significantly less potent than dialyzed normal rat serum (5,960 ± 1,400 vs. 10,800 ± 810 cpm/well; P < 0.0005 for 2.5% serum). The addition of normal rat serum (10%, vol/vol) and somatomedin-depleted (hypophysectomised) rat serum (10%), but not insulin alone, to diabetic rat serum resulted in the same degree of stimulation of DNA synthesis as that seen with normal rat serum. No evidence of an inhibitor of fibroblast DNA synthesis in untreated diabetic rat serum could be detected in this assay system. On the basis of these studies, we suggest that the defect in cellular proliferation in diabetes mellitus is due to depletion of circulating growth factors other than insulin and somatomedins. (Endocrinology 112: 1026,1983)

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Wound healing in normal and diabetic Chinese hamsters

Cited by 37 publications

References 17 publications

Effects of Hexose Sugars: Glucose, Fructose, Galactose and Mannose on Wound Healing in the Rat

Effects of Hexose Sugars: Glucose, Fructose, Galactose and Mannose on Wound Healing in the Rat

The Chinese Hamster as a Model for the Study of Diabetes Mellitus

The Effect of Streptozotocin-Induced Diabetes Mellitus on the Ability of Rat Serum to Stimulate Human Fibroblast Proliferation

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