Influence of diabetic metabolic state on fracture healing in spontaneously diabetic rats

2005 ◽  
Vol 21 (3) ◽  
pp. 288-296 ◽  
Author(s):  
Niels Follak ◽  
Ingrid Klöting ◽  
Harry Merk
Keyword(s):  
Fracture Healing ◽  
Diabetic Rats ◽  
Metabolic State ◽  
Spontaneously Diabetic Rats

Endothelins urinary excretion is increased in spontaneously diabetic rats: BB/BB

Life Sciences ◽  
1994 ◽  
Vol 56 (1) ◽  
pp. PL13-PL18 ◽  
Author(s):  
E. Morabito ◽  
N. Corsico ◽  
E. Arrigoni Martelli
Keyword(s):  
Urinary Excretion ◽  
Diabetic Rats ◽  
Spontaneously Diabetic Rats

Biomechanical evaluation of early fracture healing in normal and diabetic rats

2000 ◽  
Vol 18 (1) ◽  
pp. 126-132 ◽  
Author(s):  
James R. Funk ◽  
Joseph E. Hale ◽  
David Carmines ◽  
H. Lee Gooch ◽  
Shepard R. Hurwitz
Keyword(s):  
Fracture Healing ◽  
Diabetic Rats ◽  
Biomechanical Evaluation

Sequential Morphological Changes in Pancreatic Islets of Spontaneously Diabetic Rats

Pancreas ◽  
1990 ◽  
Vol 5 (5) ◽  
pp. 533-539 ◽  
Author(s):  
César L. A. Gómez Dumm ◽  
Maria C. Semino ◽  
Juan Jose Gagliardino
Keyword(s):  
Pancreatic Islets ◽  
Morphological Changes ◽  
Diabetic Rats ◽  
Spontaneously Diabetic Rats

scholarly journals Effects of Local Opioid Antagonist on Diabetic Fracture Rat Model

2018 ◽  
Vol 3 (3) ◽  
pp. 2473011418S0017
Author(s):  
Jarrett D. Cain ◽  
Michelle Titunick ◽  
Patricia McLaughlin ◽  
Ian Zagon
Keyword(s):  
Growth Factor ◽  
Fracture Healing ◽  
Bone Healing ◽  
Calcium Sulfate ◽  
Bone Fractures ◽  
Diabetic Rats ◽  
Receptor Expression ◽  
Opioid Antagonist ◽  
Diabetic Patients ◽  
Opioid Growth Factor

Category: Diabetes Introduction/Purpose: Complications associated with the diabetes include increased incidence of fracture healing, delayed fracture healing, delayed osteoblasts cell replication, decreased angiogenesis, migration and/or osteoblast cell differentiation. The cellular events involved in bone healing are adversely affected by diabetes; however, can be modulated by the Opioid Growth Factor (OGF)–OGF receptor (OGFr) is an inhibitory peptide that downregulates DNA synthesis in a tissue nonspecific manner. Diabetes is associated with elevated serum levels of OGF and dysregulation of the OGFr leading to multiple complications related to healing, sensitivity, and regeneration. This study explores the presence and function of the OGF-OGFr axis in bone tissue from type 1 diabetic rats examining intact and fractured femurs during early phases of the repair process Methods: Seven-week-old Sprague Dawley rats were injected with streptozotocin (40mg/kg i.p.) to induce T1D; other rats received buffer only and served as controls. After one month, hyperglycemia rats underwent surgery to produce a fracture at the distal third of the femur. Four diabetic rats received opioid antagoinist (naltrexone) and calcium sulfate and all remaining rats received calcium sulfate with water only. X-rays were taken immediately after surgery and after rats were euthanized on post-surgery; femur and tibia were collected for protein isolation, western blot analysis along with frozen or paraffin-embedded for histological analysis Results: Immunofluorescence indicated approximately 90% increase in opioid growth factor receptor expression in diabetic femurs compared to age-matched normal femurs. Western Blotting also suggested an increase in the receptor protein in diabetic bones relative to normal bone. TRAP staining for osteoclasts was greater in control and opioid antagonist-treated diabetic fractures when compared to the number of osteoclasts in vehicle-treated diabetic fractured femurs. Safranin O stained sections revealed approximately more bone in opioid growth receptor antagonist-treated diabetic bone fractures than in vehicle-treated bone fractures Conclusion: These data support our hypothesis that expression levels of OGFr are dysregulated in the bone of diabetic patients leading to complications in bone healing. Moreover, modulation of the OGF-OGFr pathway with receptor antagonists restored some aspects of bone healing. With further study, these preliminary results support the role of the OGF-OGFr axis in treatment of diabetic bone healing. New therapies to target dysregulation of the OGF-OGFr regulatory pathway in diabetes would provide a safe and effective disease-modifying treatment for delayed bone healing.

Altered regulation of cardiac glycogen metabolism in spontaneously diabetic rats

1983 ◽  
Vol 245 (4) ◽  
pp. E379-E383 ◽  
Author(s):  
T. B. Miller
Keyword(s):  
Glycogen Synthase ◽  
Glycogen Metabolism ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Metabolic Abnormalities ◽  
Insulin Deficiency ◽  
Kinase Activation ◽  
Chemically Induced ◽  
Spontaneously Diabetic Rats ◽  
Perfused Hearts

Isolated perfused hearts from control Bio-Breeding/Worcester (BB/W) rats and spontaneously diabetic BB/W rats were studied to determine whether metabolic abnormalities that are expressed in alloxan-diabetic rats in the regulation of enzymes involved in glycogen metabolism could be observed in this non-chemically induced insulin-deficient rat. Perfusion of hearts from control rats with 10(-8) M insulin for 10 min resulted in activation of glycogen synthase (30% synthase I without insulin to 44% synthase I with insulin). Perfusion of hearts from BB/W diabetic rats demonstrated a lack of acute synthase activation with insulin and a 45% decrease in synthase phosphatase activity. Perfusion of hearts from BB/W diabetic rats with 0.28 microM epinephrine for 1 min resulted in a greater activation of phosphorylase (44% phosphorylase a) than that observed in BB/W control hearts (31% phosphorylase a) perfused under the same conditions. Epinephrine produced similar changes in cyclic AMP accumulation, protein kinase activation, and phosphorylase kinase activation in perfused hearts of BB/W control and diabetic rats. Further, phosphorylase phosphatase activities were not changed by epinephrine or insulin deficiency. These studies further document metabolic abnormalities in the BB/W diabetic rat that are attributable to insulin deficiency in a non-chemically induced model for insulin-dependent diabetes.

Insulin metabolism by liver, muscle, and kidneys from spontaneously diabetic rats

1986 ◽  
Vol 250 (5) ◽  
pp. E530-E537
Author(s):  
R. Rabkin ◽  
G. M. Reaven ◽  
C. E. Mondon
Keyword(s):  
Diabetic Rats ◽  
Insulin Clearance ◽  
Immunoreactive Insulin ◽  
Insulin Metabolism ◽  
Complex Process ◽  
Consistent Manner ◽  
Liver And Kidney ◽  
Spontaneously Diabetic Rats ◽  
And Control

The in vivo metabolism of insulin is a complex process in which liver, kidney, and muscle are major participants. In this study we evaluated the effect of spontaneous hyperglycemic nonketoacidotic diabetes (DH) and ketoacidotic diabetes (DKA) on insulin clearance and degradation by these organs. Livers, hindlimbs, and kidneys from nondiabetic controls and DH and DKA Bio-Breed rats were isolated and perfused with artificial media. Liver clearance of immunoreactive insulin (ml/min) was significantly higher in DH rats, 6.0 +/- 0.2, but significantly lower in DKA rats, 3.4 +/- 0.5, compared with controls, 4.6 +/- 0.2. Acidosis alone induced by ammonium chloride loading, did not impair liver insulin clearance (4.8 +/- 0.4 ml/min). Muscle responded differently to the diabetic state in that insulin clearance was not altered by DH and DKA. Renal (organ) clearance of insulin was significantly depressed in the DKA state when compared with controls (0.52 +/- 0.04 and 0.75 +/- 0.07 ml X min-1 X g-1, respectively). This could largely be explained by a lower glomerular filtration rate. Fractional urinary insulin clearance was increased twofold above control values in DH kidneys and fourfold in DKA kidneys, indicating that tubular luminal absorption of insulin was impaired in both states. By contrast contraluminal uptake (peritubular clearance) did not differ significantly from controls. 125I-insulin degrading activity of the 100,000 g supernate fraction from muscle homogenates was similar in the diabetic and control groups. However in liver and kidney, degrading activity did not correspond to whole organ insulin clearance in a consistent manner.(ABSTRACT TRUNCATED AT 250 WORDS)

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