Paradoxical organ-specific adaptations to streptozotocin diabetes mellitus in adult rats

Pillion, Dennis J.; Jenkins, Ronald L.; Atchison, Joycelyn A.; Stockard, Cecil R.; Clements, Rex S.; Grizzle, William E.

doi:10.1152/ajpendo.1988.254.6.e749

Cited by 13 publications

(11 citation statements)

References 23 publications

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“…According to the Law of Laplace, the wall tension is increased proportionally to the diameter, which explains why the intestine will rupture outside the anastomotic line after 5 days of healing [20]. The intestine in diabetic rats is increased in length, weight and surface area [13,14]. This corresponds with the increased weight and circumference we found in the present study.…”

Section: Discussionsupporting

confidence: 76%

“…Contrary to most other organs and tissues in the diabetic rat, the intestinal tract is characterized by extensive growth in both weight and length [14]. Our study showed a marked increase in both circumference and DDW of the colon in the diabetic groups.…”

Section: Discussionsupporting

confidence: 38%

“…Verhofstad and Hendriks [11,12] have found a reduced bursting pressure of anastomoses of the intestine in animals with diabetes. However, it is well known that the intestine in diabetic rats is increased in length, weight and surface area [13,14]. As an increased circumference of the intestine will result in a reduced bursting pressure, one might speculate that this could contribute to the reduced bursting pressure found in the above-mentioned studies.…”

Section: Introductionmentioning

confidence: 91%

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Effect of Experimental Diabetes and Growth Hormone Administration on the Strength of Colonic Anastomoses in Rats

Seyer‐Hansen¹,

Andreassen²,

Christensen³

et al. 1999

Eur Surg Res

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The influence of growth hormone (GH; 2 mg/kg/day) administration on the mechanical breaking strength of colonic anastomoses in diabetic rats has been investigated on the day of operation (suture binding capacity) and after 4 and 7 days of healing. In diabetic rats, the suture binding capacity was decreased by 26% in both ultimate load and relative failure energy. After 4 days of healing, no difference was observed between control and diabetic animals. After 7 days, relative failure energy in the diabetic animals was reduced by 33%. GH administration to diabetic animals did not alter strength during the first week of healing. We found an increased circumference (33%) and defatted dry weight (22%) of the colon in diabetic rats. In conclusion, diabetes impairs the suture-binding capacity of the colon in rats, while there is only little influence on healing in the following week. GH administration could not influence the strength of colonic anastomoses in diabetic animals.

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Section: Discussionsupporting

confidence: 76%

Section: Discussionsupporting

confidence: 38%

Section: Introductionmentioning

confidence: 91%

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Effect of Experimental Diabetes and Growth Hormone Administration on the Strength of Colonic Anastomoses in Rats

Seyer‐Hansen¹,

Andreassen²,

Christensen³

et al. 1999

Eur Surg Res

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“…Hypertrophy of the small intestine musculature occurs in rats fed a diet rich in pectin (Brown et al 1979). Enlargement of the caecum is also observed in animals reared in germfree conditions (Philipps et al 1959;FaIk 1960), in relation to the absence of intestinal flora (Gordon 1959), and in diabetic animals (Pillion et al 1988). The histology of the caecal musculature has not yet been studied, but we have observed that in rats fed with a high-fibre diet, or born and bred in germ-free conditions, or affected by streptozotocin diabetes, the enlargement of the caecum is accompanied by a moderate thickening of its wall and thus involves a process of hypertrophy.…”

Section: Experimental Models In Laboratory Animalsmentioning

confidence: 98%

Hypertrophy of visceral smooth muscle

Gabella

1990

Anat Embryol

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Smooth muscles of viscera undergo a large increase in volume when there is a chronic, partial obstruction impairing the flow of lumenal contents. Hypertrophy of smooth muscle occurs in various medical conditions and several methods are available for inducing it experimentally in laboratory animals, especially in urinary bladder, small intestine and ureter. The hypertrophic response differs somewhat with the type of organ, the animal species, the age of the subject, and the experimental procedure. Ten- to fifteen-fold increases in muscle volume develop within a few weeks in the urinary bladder or the ileum of adult animals, a growth that would not have occurred in the lifespan of the animal without the experimental intervention. The general architecture of the muscle and the boundaries with adjacent tissues are well preserved. In intestinal hypertrophy, muscle cells increase in number: mitoses are found in mature, fully differentiated muscle cells. Cell division by full longitudinal splitting of muscle cells may also occur. Enlargement of muscle cells accounts for most of the muscle hypertrophy. The hypertrophic muscle cell has an irregular profile with deep indentations of the cell membrane, bearing caveolae and dense bands; however, the cell surface grows less than the cell volume (reduction of surface-to-volume ratio). The nucleus is crenated and is much less enlarged than the cell (reduction of the nucleo-plasmatic ratio). Mitochondria grow in number but in some muscles their spatial density decreases; intermediate filaments increase more than myofilaments. The spatial density of sarcoplasmic reticulum is generally increased. In the hypertrophic intestine, gap junctions increase in number and size; in the bladder, gap junctions are absent both in control and in hypertrophy. Thus the hypertrophic muscle cell is not only larger than a control cell, but has a different pattern of its structural components. Extensive neo-angiogenesis maintains a good blood supply to the hypertrophic muscle. The density of innervation is much decreased in the hypertrophic intestine, whereas it appears well maintained in the bladder. Neuronal enlargement is found in the intramural ganglia of the intestine and in the pelvic ganglion. The mechanisms involved in hypertrophic growth are unknown. Three possible factors, mechanical factors, especially stretch, altered nerve discharge, and trophic factors are discussed.

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“…Overall growth, as measured by carcass weight and skeletal size parameters, was impaired. How ever, internal organs were relatively spared, except for the kidney, as was noted in pre vious studies [3,8], There is controversy in the literature about whether this is an effect o f the drug per se [17][18][19], The majority o f the discrepancy in weight between the STZtreated and control fetuses was accounted for by the differences in carcass weight.…”

Section: Discussionmentioning

confidence: 91%

Effect of Hypoinsulinemia on Growth in the Fetal Rabbit

Chaffin¹,

Clark

Mccracken

et al. 1995

Neonatology

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Insulin is an important regulatory hormone in the control of fetal growth. In a fetal rabbit model, a non-ruminant species, the effects of insulin deprivation on glucose, growth and protein metabolism were studied. The fetuses of 10 pregnant New Zealand white rabbits in one uterine horn received a subcutaneous injection on day 25 of gestation (term = 30 days) of 0.1 mg streptozotocin (STZ)/gm fetal weight. The fetuses in the opposite horn received a sham injection of buffer. The dams were then killed on day 29. The fetal insulin concentration was depressed by 38%, and the serum glucose concentration was elevated by 28% in animals given STZ when compared to control animals. Fetal weights, carcass weights and skeletal growth, as measured by crown-rump length and tibial length of STZ-treated fetuses, were significantly reduced by 7–13%. However, organ weights were not significantly different, except for the kidneys which were 17% lighter. Protein and mineral contents of the carcasses were also reduced compared to the control fetuses. Thus, insulin deprivation in fetal rabbits results in significant growth impairment in a pattern similar to that of human asymmetric intrauterine growth retardation.

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Paradoxical organ-specific adaptations to streptozotocin diabetes mellitus in adult rats

Cited by 13 publications

References 23 publications

Effect of Experimental Diabetes and Growth Hormone Administration on the Strength of Colonic Anastomoses in Rats

Effect of Experimental Diabetes and Growth Hormone Administration on the Strength of Colonic Anastomoses in Rats

Hypertrophy of visceral smooth muscle

Effect of Hypoinsulinemia on Growth in the Fetal Rabbit

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