scholarly journals Effects of vitamin A deficiency and repletion on rat insulin secretion in vivo and in vitro from isolated islets.

1987 ◽  
Vol 79 (1) ◽  
pp. 163-169 ◽  
Author(s):  
B S Chertow ◽  
W S Blaner ◽  
N G Baranetsky ◽  
W I Sivitz ◽  
M B Cordle ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Isolated Islets ◽  
Insulin Secretion In Vivo

scholarly journals Cellular basis of urothelial squamous metaplasia

2005 ◽  
Vol 171 (5) ◽  
pp. 835-844 ◽  
Author(s):  
Feng-Xia Liang ◽  
Maarten C. Bosland ◽  
Hongying Huang ◽  
Rok Romih ◽  
Solange Baptiste ◽  
...  
Keyword(s):  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Squamous Metaplasia ◽  
Culture Conditions ◽  
Growth Potential ◽  
Basal Cells ◽  
Cellular Basis ◽  
Proximal Urethra

Although the epithelial lining of much of the mammalian urinary tract is known simply as the urothelium, this epithelium can be divided into at least three lineages of renal pelvis/ureter, bladder/trigone, and proximal urethra based on their embryonic origin, uroplakin content, keratin expression pattern, in vitro growth potential, and propensity to keratinize during vitamin A deficiency. Moreover, these cells remain phenotypically distinct even after they have been serially passaged under identical culture conditions, thus ruling out local mesenchymal influence as the sole cause of their in vivo differences. During vitamin A deficiency, mouse urothelium form multiple keratinized foci in proximal urethra probably originating from scattered K14-positive basal cells, and the keratinized epithelium expands horizontally to replace the surrounding normal urothelium. These data suggest that the urothelium consists of multiple cell lineages, that trigone urothelium is closely related to the urothelium covering the rest of the bladder, and that lineage heterogeneity coupled with cell migration/replacement form the cellular basis for urothelial squamous metaplasia.

In vivo and in vitro Study of the Effects of Vitamin A Deficiency on Rat Third Molar Development

1986 ◽  
Vol 65 (12) ◽  
pp. 1445-1448 ◽  
Author(s):  
S.S. Harris ◽  
J.M. Navia
Keyword(s):  
Vitamin A ◽  
Organ Culture ◽  
Culture System ◽  
Vitamin A Deficiency ◽  
Third Molar ◽  
In Vitro Study ◽  
Organ Culture System ◽  
Vitamin A Status

We have examined the effect of in vivo vitamin A status on subsequent rat third molar formation and mineralization in an in vitro organ culture system. Vitamin A deficiency imposed during an eight-day in vitro period caused effects very similar to those of vitamin A deficiency imposed on rats in vivo. Analysis of the data also demonstrates that retinoic acid is capable of reversing the interference in mineralization of third molars induced by vitamin A deficiency in the organ culture system.

Transgenic overexpression of intraislet ghrelin does not affect insulin secretion or glucose metabolism in vivo

2012 ◽  
Vol 302 (4) ◽  
pp. E403-E408 ◽  
Author(s):  
Mika Bando ◽  
Hiroshi Iwakura ◽  
Hiroyuki Ariyasu ◽  
Hiroshi Hosoda ◽  
Go Yamada ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Glucose Metabolism ◽  
Medium Chain Triglyceride ◽  
Physiological Role ◽  
Standard Diet ◽  
Entry Site ◽  
Insulin Secretion In Vivo

Whereas ghrelin is produced primarily in the stomach, a small amount of it is produced in pancreatic islets. Although exogenous administration of ghrelin suppresses insulin secretion in vitro or in vivo, the role of intraislet ghrelin in the regulation of insulin secretion in vivo remains unclear. To understand the physiological role of intraislet ghrelin in insulin secretion and glucose metabolism, we developed a transgenic (Tg) mouse model, rat insulin II promoter ghrelin-internal ribosomal entry site-ghrelin O-acyl transferase (RIP-GG) Tg mice, in which mouse ghrelin cDNA and ghrelin O-acyltransferase are overexpressed under the control of the rat insulin II promoter. Although pancreatic desacyl ghrelin levels were elevated in RIP-GG Tg mice, pancreatic ghrelin levels were not altered in animals on a standard diet. However, when Tg mice were fed a medium-chain triglyceride-rich diet (MCTD), pancreatic ghrelin levels were elevated to ∼16 times that seen in control animals. It seems likely that the gastric ghrelin cells possess specific machinery to provide the octanoyl acid necessary for ghrelin acylation but that this machinery is absent from pancreatic β-cells. Despite the overexpression of ghrelin, plasma ghrelin levels in the portal veins of RIP-GG Tg mice were unchanged from control levels. Glucose tolerance, insulin secretion, and islet architecture in RIP-GG Tg mice were not significantly different even when the mice were fed a MCTD. These results indicate that intraislet ghrelin does not play a major role in the regulation of insulin secretion in vivo.

scholarly journals 91 SALICYLATE INTOXICATION AND INSULIN SECRETION: “IN VIVO” AND “IN VITRO” STUDIES

1981 ◽  
Vol 15 (2) ◽  
pp. 198-198
Author(s):  
J C Basabe ◽  
L Bruno ◽  
E Alvarez ◽  
M E Fernández ◽  
E Astolfi
Keyword(s):  
Insulin Secretion ◽  
In Vitro Studies ◽  
Insulin Secretion In Vivo ◽  
Salicylate Intoxication

scholarly journals Vitamin A and the biosynthesis of sulphated mucopolysaccharides. Experiments with rats and cultured neoplastic mast cells

1969 ◽  
Vol 111 (4) ◽  
pp. 407-412 ◽  
Author(s):  
D. B. Thomas ◽  
C A Pasternak
Keyword(s):  
Growth Rate ◽  
Mast Cells ◽  
Vitamin A ◽  
Uronic Acid ◽  
Vitamin A Deficiency ◽  
Horse Serum ◽  
Vitamin A Status ◽  
Uronic Acid Content

1. The uptake and incorporation of [35S]sulphate into mucopolysaccharides by colon and duodenum in vitro are unaffected by the vitamin A status of the animals. 2. Uptake and incorporation in vivo are unaffected at 4hr. after injection of [35S]sulphate, but at later times are decreased in some tissues of vitamin A-deficient animals. 3. The rate of removal of 35S from blood, its rate of appearance in urine, the plasma concentration of sulphate and the uronic acid content of several tissues are not significantly altered in vitamin A deficiency. 4. These results, and direct measurement of 35S in mucopolysaccharides at various times after injection of [35S]sulphate, suggest that the synthesis of mucopolysaccharides is unaffected but that their turnover is increased in vitamin A deficiency. 5. Neither the growth rate of, nor the incorporation of [35S]sulphate into heparin by, P815Y and HC cultured neoplastic mast cells is decreased when the horse serum necessary for growth is treated with ultraviolet light or is replaced by serum from vitamin A-deficient rats. 6. The addition of citral is no more toxic to growth rate or to incorporation of 35S than is the addition of vitamin A itself. 7. It is concluded that neoplastic mast cells in culture do not require vitamin A for growth or for the synthesis of heparin. 8. None of these results is compatible with the view that vitamin A or a derivative is directly involved in the biosynthesis of sulphated mucopolysaccharides.

Neuroendocrine regulatory peptide-2 stimulates glucose-induced insulin secretion in vivo and in vitro

2012 ◽  
Vol 428 (4) ◽  
pp. 512-517 ◽  
Author(s):  
Abu Saleh Md. Moin ◽  
Hideki Yamaguchi ◽  
Marie Rhee ◽  
Ji-Wom Kim ◽  
Koji Toshinai ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Regulatory Peptide ◽  
Insulin Secretion In Vivo

Effects of a 7-day infusion of glucose on insulin secretion in vivo and in vitro in ventromedial hypothalamic-lesioned obese rats

1998 ◽  
Vol 35 (1) ◽  
pp. 26-33 ◽  
Author(s):  
M. Kuboi ◽  
M. Egawa ◽  
N. Udaka ◽  
T. Ito ◽  
S. Inoue ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Insulin Secretion In Vivo ◽  
Obese Rats
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