Effect of glucose on insulin biosynthesis and β cell ultrastructure in cultured fetal rat pancreas

1984 ◽  
Vol 100 (2) ◽  
pp. 155-160 ◽  
Author(s):  
R. D. G. Milner ◽  
A. Cser ◽  
G. H. Cope
Keyword(s):  
Cell Ultrastructure ◽  
Insulin Biosynthesis ◽  
Cell Nuclei ◽  
Β Cell ◽  
Absolute Volume ◽  
Fetal Rat ◽  
Insulin Granules ◽  
Fetal Rats ◽  
Exocrine Cell

ABSTRACT Pancreatic rudiments from 14-day fetal rats were cultured whole for 8 days in medium containing 5·5 or 16·5 mmol glucose/l (1G or 3G medium). Rudiments grown in 3G medium (3G cells) contained more DNA and insulin than those grown in 1G medium (1G cells) but there was no alteration in the insulin/DNA ratio or the fractional area of the rudiment occupied by insulin-containing cells. Morphometric analysis of ultrastructure revealed that the β cells grown in 3G medium were smaller and had smaller nuclei than those grown in 1G medium. The size of exocrine cell nuclei in 1G or 3G medium was similar. Insulin granules occupied a greater proportion of the cytoplasmic volume in rudiments grown in 3G medium although the mean absolute volume of insulin granules per cell grown in 1G and 3G media was similar. Hence the residual cytoplasmic volume (cell—nucleus and granules) of 3G cells was less than that of 1G cells. Insulin granules from 3G cells had smaller granule sacs and cores than those from 1G cells. It is concluded that glucose stimulates the growth of rat fetal pancreas in vitro and has important effects on β cell ultrastructure. J. Endocr. (1984) 100, 155–160

Stimulation of aromatase activity in the fetal rat testis by cyclic AMP and FSH

1988 ◽  
Vol 118 (3) ◽  
pp. 485-489 ◽  
Author(s):  
J.-P. Weniger ◽  
A. Zeis
Keyword(s):  
Cyclic Amp ◽  
Specific Activity ◽  
Isotopic Dilution ◽  
Aromatase Activity ◽  
Dibutyryl Cyclic Amp ◽  
Rat Testis ◽  
Fetal Rat ◽  
Fetal Rats ◽  
Stimulation Of

ABSTRACT The effect of dibutyryl cyclic AMP and FSH on oestrogen biosynthesis was investigated in testes from 18- to 21-day-old fetal rats cultured in vitro in the presence of tritiated testosterone. Oestrone and oestradiol concentrations were measured by determination of constant specific activity after isotopic dilution. Dibutyryl cyclic AMP and FSH markedly stimulated the conversion of testosterone into both oestrone and oestradiol at all stages studied. Oestradiol synthesis was stimulated by two- to sevenfold, while stimulation of oestrone synthesis was even greater. The results demonstrate that the aromatase enzyme system of the fetal rat testis responds to cyclic AMP and FSH. J. Endocr. (1988) 118, 485–489

scholarly journals Tropism Analysis of Two Coxsackie B5 Strains Reveals Virus Growth in Human Primary Pancreatic Islets but not in Exocrine Cell Clusters In Vitro

2013 ◽  
Vol 7 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Hodik M ◽  
Lukinius A ◽  
Korsgren O ◽  
Frisk G
Keyword(s):  
Endocrine Cells ◽  
Close Association ◽  
Post Inoculation ◽  
Virus Growth ◽  
Virus Particles ◽  
Cell Clusters ◽  
Pancreatic Cells ◽  
Insulin Granules ◽  
Exocrine Cell

Human Enteroviruses (HEVs) have been implicated in human pancreatic diseases such as pancreatitis and type 1 diabetes (T1D). Human studies are sparse or inconclusive and our aim was to investigate the tropism of two strains of Coxsackie B virus 5 (CBV-5) in vitro to primary human pancreatic cells. Virus replication was measured with TCID50 titrations of aliquots of the culture medium at different time points post inoculation. The presence of virus particles or virus proteins within the pancreatic cells was studied with immunohistochemistry (IHC) and electron microscopy (EM). None of the strains replicated in the human exocrine cell clusters, in contrast, both strains replicated in the endocrine islets of Langerhans. Virus particles were found exclusively in the endocrine cells, often in close association with insulin granules. In conclusion, CBV-5 can replicate in human endocrine cells but not in human exocrine cells, thus they might not be the cause of pancreatitis in humans. The association of virus with insulin granules might reflect the use of these as replication scaffolds.

Respiratory and locomotor patterns generated in the fetal rat brain stem-spinal cord in vitro

1992 ◽  
Vol 67 (4) ◽  
pp. 996-999 ◽  
Author(s):  
J. J. Greer ◽  
J. C. Smith ◽  
J. L. Feldman
Keyword(s):  
Spinal Cord ◽  
Brain Stem ◽  
Cellular Mechanisms ◽  
Motor Patterns ◽  
Rhythmic Motor ◽  
Fetal Rat ◽  
Fetal Rats ◽  
Locomotor Patterns ◽  
Fetal Rat Brain

An in vitro brain stem-spinal cord preparation from last trimester (E13-E21) fetal rats, which generates rhythmic respiratory and locomotor patterns, is described. These coordinated motor patterns emerge at stages E17-E18. Synchronous rhythmic motor activity, not clearly characterized as respiratory or locomotor, can occur as early as E13. With this preparation, it is now possible to study the ontogenesis of circuits and cellular mechanisms underlying these critical movements.

Glucose-coupled sodium absorption in the developing rat colon

1986 ◽  
Vol 250 (2) ◽  
pp. G221-G226 ◽  
Author(s):  
G. D. Potter ◽  
S. M. Burlingame
Keyword(s):  
Amino Acid ◽  
Dry Weight ◽  
Rat Colon ◽  
Sodium Absorption ◽  
Na Transport ◽  
Fetal Rat ◽  
Fetal Rats ◽  
The Difference ◽  
Developing Rat

The developing mammalian colon is lined by villi and is capable of glucose and amino acid absorption at birth in the rat. Neither the point at which this capacity is lost nor the effect of the capacity for glucose transport on Na absorption has been studied. We have now applied a system for perfusion of the lumen of in vitro segments of colon from 20-day-old fetal rats, and pups between 6 and 8 days old, to measure Na transport and transepithelial potential difference (PD). The lumens of colons from animals at both ages were perfused with solutions containing glucose or mannitol and 22Na. Net Na transport was 164 +/- 37 mu eq X h-1 X g dry weight tissue perfused-1, as determined by the difference between lumen-to-bath and bath-to-lumen flux in fetal rat colons at day 20. Glucose increased the lumen-to-bath flux by 90 +/- 35 mu eq X h-1 X g-1. PD was immediately increased from -1.7 +/- 0.16 to -8.0 +/- 0.96 mV (lumen with respect to bath) by the addition of glucose, and the change in PD was inhibited by 10(-4) M phlorizin. The PD response to glucose was lost at day 2 of life, but the villus epithelium persisted. Amiloride, 10(-4) M, did not alter PD or Na transport at either age. We conclude that the fetal rat colon exhibits glucose-dependent Na flux at birth but that this property is lost by 6-8 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Stimulation of aromatase activity in the fetal rat gonads by cAMP and FSH

1988 ◽  
Vol 119 (3) ◽  
pp. 381-385 ◽  
Author(s):  
J.-P. Weniger ◽  
A. Zeis
Keyword(s):  
Specific Activity ◽  
Isotopic Dilution ◽  
Aromatase Activity ◽  
Fetal Rat ◽  
Estrogen Synthesis ◽  
Fetal Rats ◽  
Stimulation Of ◽  
Constant Specific Activity

Abstract. The gonads from 17- to 21-day-old fetal rats were cultured in vitro in the presence of [3H]testosterone and in the presence or absence of cAMP or FSH, and estrone and estradiol formed were measured by double isotopic dilution and recrystallization to constant specific activity. Estrogen synthesis by testes was stimulated by both cAMP and FSH as early as at 18 days of gestation. FSH did not enhance aromatase activity in ovaries, although cAMP did. It is remarkable that FSH controls estrogen synthesis in the testis earlier than in the ovary.

Responsiveness of vitamin D-deficient fetal rat limb bones to parathyroid hormone in culture

1983 ◽  
Vol 244 (4) ◽  
pp. E421-E424
Author(s):  
P. H. Stern ◽  
B. P. Halloran ◽  
H. F. DeLuca ◽  
T. J. Hefley
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Additive Model ◽  
Vitamin D Status ◽  
Dihydroxyvitamin D3 ◽  
Limb Bones ◽  
Fetal Rat ◽  
Fetal Rats

Radii and ulnae from 19-day fetal rats from normal or vitamin D-deficient mothers were treated with 25-hydroxyvitamin D3, 1,25-dihydroxyvitamin D3, or parathyroid hormone in vitro. Both sets of bones resorbed in response to all three agents. Statistical analysis indicated a purely additive model for the effects of vitamin D status and the bone-resorbing agents, with no evidence for interaction. The results suggest that the impaired calcemic response to parathyroid hormone seen in vitamin D-deficient animals in vivo is not the result of a specific unresponsiveness of vitamin D-deficient bone to parathyroid hormone.

EFFECT OF NON-ESSENTIAL AMINO ACIDS ON FETAL RAT PANCREATIC GROWTH AND INSULIN SECRETION IN VITRO

1981 ◽  
Vol 91 (2) ◽  
pp. 289-297
Author(s):  
R. D. G. MILNER ◽  
M. DE GASPARO
Keyword(s):  
Amino Acids ◽  
Culture Medium ◽  
Total Concentration ◽  
Essential Amino Acids ◽  
Insulin Biosynthesis ◽  
Quantitative Morphology ◽  
Pancreatic Growth ◽  
Fetal Rat ◽  
Insulin Secretion In Vitro

Fetal rat pancreatic rudiments explanted on day 14 of gestation were grown for 6 days in organ culture in medium containing glucose (5·5 or 16·5 mmol/l) and essential amino acids (3·5 or 13·1 mmol/l). Non-essential amino acids (alanine, aspartic acid, asparagine, glycine, proline and serine) were added to the culture medium in a number of combinations and at a maximum total concentration of 4·0 mmol/l. At the end of the period of culture rudiments were compared for DNA content, insulin concentration and quantitative morphology. The release of insulin from the rudiments was tested during 6-h incubations on day 6 of culture. Enrichment of the culture medium with any combination of non-essential amino acids had a slight or no effect on the growth or cellular composition of the rudiment or insulin release from it. Addition of all the non-essential amino acids to medium containing 16·5 mmol glucose and 13·1 mmol essential amino acids/l caused a dramatic reduction in the net insulin accumulation by the cultured rudiment. Combinations of non-essential amino acids in which one or more were omitted did not have the same effect. These findings suggest that fetal rat pancreas grown in vitro may require both essential and non-essential amino acids for the full expression of insulin biosynthesis and secretion.

Erythroid colony formation by fetal rat liver and spleen cells in vitro: inhibition by a low relative molecular mass component of fetal spleen

Development ◽  
1992 ◽  
Vol 114 (1) ◽  
pp. 213-219
Author(s):  
M.D. Nagel ◽  
J. Nagel
Keyword(s):  
Molecular Mass ◽  
Lethal Effect ◽  
Relative Molecular Mass ◽  
Spleen Cells ◽  
Fetal Rat ◽  
Fetal Rats ◽  
Percoll Gradients ◽  
Fetal Rat Liver ◽  
Liver Fraction

Liver and spleen hematopoietic cell suspensions from 20-day-old-fetal rats were fractionated on Percoll gradients. A granulocyte-rich splenic fraction inhibited CFUe production by cultures of a CFUe-enriched liver fraction, and by cultures of unfractionated liver and spleen hematopoietic cells. Conditioned medium from the spleen cell fraction contained an inhibitor of relative molecular mass, Mr, 25–35 × 10(3). The sensitivity of spleen cells to the inhibitor varied with the age of the fetus from which they were derived (20-day-old less than 18-and 19-day-old). No such age-dependence was found for liver cells. The inhibitor affects cycling CFUe, blocks the lethal effect of AraC, does not appear to be lineage-specific and its influence can be reversed by washing.

Purified bovine AMH induces a characteristic freemartin effect in fetal rat prospective ovaries exposed to it in vitro

Development ◽  
1987 ◽  
Vol 100 (1) ◽  
pp. 43-55 ◽  
Author(s):  
B. Vigier ◽  
F. Watrin ◽  
S. Magre ◽  
D. Tran ◽  
N. Josso
Keyword(s):  
Epithelial Cells ◽  
Germ Cell ◽  
Sertoli Cells ◽  
Basal Membrane ◽  
Cell Depletion ◽  
Morphological Abnormalities ◽  
Fetal Rat ◽  
Fetal Rats ◽  
Clear Cytoplasm

To determine whether anti-Mullerian hormone (AMH) is responsible for the gonadal lesions observed in bovine genetic females united by placental anastomoses to male twins (freemartins), prospective ovaries of fetal rats were exposed to purified bovine AMH in vitro. In cultures initiated at 14 days p.c. and maintained 3 to 10 days, AMH consistently induced a characteristic ‘freemartin effect’, namely reduction of gonadal volume, germ cell depletion and differentiation, in the gonadal blastema, of epithelial cells with large clear cytoplasm linked by interdigitations, resembling rat fetal Sertoli cells. These cells tend to become polarized and form cords, delineated by a continuous basal membrane containing laminin and fibronectin. Such structures, resembling developing seminiferous cords, were not detected in control ovarian cultures. These data strongly suggest that AMH is the testicular factor responsible for triggering the morphological abnormalities of freemartin gonads.

scholarly journals Antipsychotic olanzapine-induced misfolding of proinsulin in the endoplasmic reticulum accounts for atypical development of diabetes

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Satoshi Ninagawa ◽  
Seiichiro Tada ◽  
Masaki Okumura ◽  
Kenta Inoguchi ◽  
Misaki Kinoshita ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Bond Formation ◽  
Insulin Biosynthesis ◽  
Β Cell ◽  
Cell Dysfunction ◽  
Subsequent Decrease ◽  
Insulin Granules ◽  
Second Generation Antipsychotics ◽  
Atypical Development ◽  
Primary Localization

Second-generation antipsychotics are widely used to medicate patients with schizophrenia, but may cause metabolic side effects such as diabetes, which has been considered to result from obesity-associated insulin resistance. Olanzapine is particularly well known for this effect. However, clinical studies have suggested that olanzapine-induced hyperglycemia in certain patients cannot be explained by such a generalized mechanism. Here, we focused on the effects of olanzapine on insulin biosynthesis and secretion by mouse insulinoma MIN6 cells. Olanzapine reduced maturation of proinsulin, and thereby inhibited secretion of insulin; and specifically shifted the primary localization of proinsulin from insulin granules to the endoplasmic reticulum. This was due to olanzapine’s impairment of proper disulfide bond formation in proinsulin, although direct targets of olanzapine remain undetermined. Olanzapine-induced proinsulin misfolding and subsequent decrease also occurred at the mouse level. This mechanism of olanzapine-induced β-cell dysfunction should be considered, together with weight gain, when patients are administered olanzapine.

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