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Y Stefan

Publications and source records attributed to Y Stefan.

At least 19 recordsLinked to original sources
PubMed1987

Stimulation of insulin secretion reveals heterogeneity of pancreatic B cells in vivo.

We examined the immunofluorescence and ultrastructural changes of insulin-producing B cells in the center and at the periphery of islets of Langerhans during in vivo stimulation by glucose and glibenclamide. A decreased insulin immunostaining was detected in islets from the splenic rat pancreas after 1.5 h of glucose stimulation. By contrast, immunofluorescence changes became apparent in islets from the duodenal pancreas only after greater than 3 h of hyperglycemia. In both cases, the immunolabeling of central B cells decreased before that of peripheral B cells. Similar changes were seen following in vivo stimulation of insulin secretion by glibenclamide. At the ultrastructural level, hyperglycemia decreased the volume density of B cell secretory granules and increased that of rough endoplasmic reticulum and Golgi apparatus. These changes were also detected earlier in central than in peripheral B cells and earlier in splenic than in duodenal islets. The data show that B cells form a heterogeneous population in vivo.

Animals↗
PubMed1986

Loss of insulin response to glucose but not arginine during the development of autoimmune diabetes in BB/W rats: relationships to islet volume and glucose transport rate.

The insulin and glucagon responses to 10 mM glucose and 10 mM arginine were studied in pancreata isolated from nondiabetic diabetes-prone and diabetes-resistant BB/W rats at 60, 80, and 140 days of age and in diabetic BB/W rats on the 1st and 14th days of their diabetes. In the former group the insulin response to glucose declined progressively with age (r = -0.575; P less than 0.01) and at 140 days was significantly below age-matched diabetes-resistant controls (P less than 0.05). The insulin response to arginine did not decline with age in either group. For diabetic rats, on the first day of the diabetes, the insulin response to glucose was absent but the response to arginine did not differ from nondiabetic controls. On day 14 responses to glucose and arginine were both absent. The glucagon response to arginine showed no trend despite a decline in baseline glucagon secretion. Endocrine tissue in nondiabetic diabetes-prone rats made up 0.8 +/- 0.2% of the pancreas at 60 days of age and 0.52 +/- 0.22% at 140 days of age; the latter was significantly less than in 140-day-old diabetes-resistant controls (P less than 0.05). In diabetic rats on the 1st and 14th days of diabetes endocrine tissue was 0.2 +/- 0.1% and 0.07 +/- 0.02%, respectively. The glucose transport rate in islets isolated on the first day of diabetes was profoundly reduced compared to age-matched nondiabetic diabetes-prone controls. Thus, a population of arginine-responsive, glucose-unresponsive islets with low glucose transport rates is present at the onset of overt diabetes in BB/W rats.

Age Factors↗
PubMed1985

Beckwith-Wiedemann syndrome: a quantitative, immunohistochemical study of pancreatic islet cell populations.

The endocrine cell content of the pancreas of two cases of Beckwith-Wiedemann syndrome with islet cell adenomatosis were studied. Insulin, glucagon, somatostatin and pancreatic polypeptide cells were evaluated qualitatively and quantitatively with the indirect immunofluorescence method and morphometry was used to establish the volume density of the four endocrine cell populations. This evaluation showed a marked increase of insulin and glucagon cells and a lesser augmentation of pancreatic polypeptide cells and somatostatin cells. However, the percent of somatostatin cells was decreased in comparison with controls. Qualitatively, the two pancreas were characterized by the lack of segregation of glucagon and pancreatic polypeptide cells to distinct parts of the gland, with each cell type being abundant in the pancreatic region in which they are normally very sparse. The marked increase of endocrine cells often took the form of giant islet-like structures formed by smaller subunits; however, despite this increase, the distribution of insulin cells respected the normal pattern, i.e. clusters of B cells surrounded by non-B cells. These findings indicate that besides the proliferation of pancreatic endocrine cells maintaining a normal topographical distribution of B versus non-B cells, the pancreas of patients with the Beckwith-Wiedemann syndrome may have undergone abnormal development with a consequent lack of segregation of glucagon and pancreatic polypeptide cells to different parts of the gland.

Beckwith-Wiedemann Syndrome↗
PubMed1983

A quantitative immunofluorescent study of the endocrine cell populations in the developing human pancreas.

The immunofluorescent cell content of the pancreas of 8--40-wk fetuses and of 1.5--5-mo Caucasian infants was quantitatively evaluated using anti-insulin, anti-glicentin, anti-glucagon, anti-somatostatin, and anti-pancreatic polypeptide antisera. The most significant findings are: (1) the pancreas of 8--10 wk fetuses contains a sizable population of endocrine cells reacting exclusively to anti-glicentin antiserum. This cell population decreases and disappears in later stages and is replaced by the adult type glucagon/glicentin immunoreactive cell; (2) the pancreatic polypeptide-rich region shows a lower relative endocrine cell content as compared with the glucagon-rich region and its islets appear smaller; (3) in the total pancreas, the relative (volume density) and absolute (microliter) insulin cell content increases regularly with age, while the relative volume of glucagon cells peaks in fetal life (wk 17--20) to decrease in infants, although remaining at higher levels than in adults; the relative and absolute volumes of somatostatin cells are elevated in fetal and infant stages studied where they represent the second most abundant cell type, while pancreatic polypeptide cells appear to least abundant cells during prenatal and infant life. These data show several differences with the pattern of the respective endocrine cell populations in the adult pancreas.

Female↗
PubMed1982

Glicentin precedes glucagon in the developing human pancreas.

A quantitative evaluation of immunofluorescence elicited by anti-insulin, anti-glucagon, anti-glicentin, anti-somatostatin and anti-pancreatic polypeptide antisera has been carried out in the pancreas of 5 human fetuses from 3.0 to 9.6 cm C.R. The data obtained indicate that while insulin and somatostatin-containing cells are approximately in similar proportions with respect to the other endocrine cell types in the five fetuses studied, the glucagon and glicentin immunoreactive cells and the pancreatic polypeptide cells are not : a) pancreatic polypeptide-containing cells increase in proportion as fetuses grow older; b) the youngest fetuses (3.0 to 4.3 cm C.R.) contain a high proportion of cells reacting to anti-glicentin antiserum only (GLI-cells) and a small proportion of cells stained both with the anti-glicentin and anti-glucagon antisera (GLI/GLU-cells). However, the latter cell type which stains similarly as the postnatal and adult pancreatic A-cell (GLI-cells are not detectable in the postnatal and adult pancreas) increases iin proportion in older fetuses, while the proportion of GLI-cells decrease. The data suggest that the definitive adult-type A-cell matures from a GLI-cell type which is not able to convert glucagon precursors GLI(s) into glucagon.

Female↗
PubMed1982

Quantitation of endocrine cell content in the pancreas of nondiabetic and diabetic humans.

The application of immunofluorescence technique with anti-insulin, anti-glucagon, anti-somatostatin, and anti-pancreatic polypeptide (PP) antisera to sections of precisely sampled regions of the human pancreas allowed the quantitative evaluation of the total content of these four endocrine cell populations in 13 nondiabetics, in 2 insulin-dependent diabetics (IDDM), and in 2 non-insulin-dependent diabetic subjects (NIDDM) of various age and sex. In nondiabetic subjects, PP-cells appear sex-related. Male individuals have a significantly greater volume of PP-cells than female. In diabetic subjects, the only marked difference as compared with nondiabetics is the reduction of insulin cell volume in IDDM. Other small differences between individual endocrine cell volumes are detectable in both IDDM and NIDDM as compared with nondiabetics, but their significance is at present unclear. The qualitative changes of islet structure accompanying insulin cell reduction in IDDM were not considered in the present study.

Adolescent↗
PubMed1981

Primitive islets contain two populations of cells with differing glucagon immunoreactivity.

Immunofluorescence staining with insulin, glucagon, and somatostatin antisera revealed different immunoreactive cell types in the pancreatic islets of the ratfish. In particular, one cell type was present that reacted with C- and N-terminal anti-glucagon sera, while another type was only detected by N-terminal anti-glucagon sera. The latter cell, however, became reactive to C-terminal anti-glucagon after proteolytic treatment of the section. A similar cell type was found in the epithelium of the pancreatic duct and of the gastrointestinal mucosa. The data indicate that among glucagon immunoreactive cells, some cells situated exclusively in the pancreas possess both C- and N-terminal glucagon immunoreactants, while in other pancreatic as well as intestinal cells, the sequence that binds C-terminal anti-glucagon serum appears masked and becomes accessible to the antibody only after proteolytic digestion.

Animals↗
PubMed1979

Pancreatic fat.

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Adipose Tissue↗
PubMed1979

Identification of a lobe in the adult human pancreas rich in pancreatic polypeptide.

Systematic sampling of human necropsy pancreases has revealed that pancreatic polypeptide (PP) cells are not distributed equally in the gland. PP-cells are the most abundant cell type in the posterior part of the pancreatic head while they are scarce or absent in the remainder of the gland. The PP-rich part of the head can be separated by blunt dissection from the pancreas as a discrete lobe. This lobe probably originates from the ventral pancreatic bud during embryogenesis. A quantitative study of the immunofluorescent endocrine cell types (insulin, glucagon, somatostatin and pancreatic polypeptide cells) in PP-rich and PP-poor regions of pancreases in 8 subjects with ages ranging from 33 fetal weeks to 80 years, showed that the proportions of the cell types were different in youngs and adults.

Adult↗
PubMed1978

[Immunofluorescent demonstration of pancreatic polypeptide (PP) in pancreas and digestive tube of bony and cartilaginous fish].

When antisera specific against bovine PP (BPP) were used, immunoreactive parenchymal cells were observed in the endocrine pancreas and in the gastro-intestinal tract of the teleost bony fish Cottus scorpius, as well as in the pancreas of the elasmobranchian cartilaginous fish Squalus acanthias. Of the two principal islets of Cottus, PP-cells were located selectively to that in the pyloric region.

Animals↗
PubMed1978

Virus-induced diabetes in mice: a quantitative evaluation of islet cell population by immunofluorescence technique.

The endocrine cell populations of pancreatic islets in encephalomyocarditis (EMC)-virus infected mice were assessed quanititatively by immunofluorescence using specific antisera against 4 islet hormones. A marked reduction of the volume of insulin-containing (B-) cells (up to one tenth of control values) was observed at all stages studied in the hyperglycaemic mice. This was accompanied by the inversion of the normal ratio between B- and non B-cells. The volume of the latter cell types was also modified at different time points after infection: glucagon-cells were augmented 14 days after infection; PP-cells were decreased 2--3 days and 21 days after infection; somatostatin-cells decreased to one-fourth of control values in hyperglycaemic animals 21 days after infection. The latter results suggest that non B-cells are also involved in islet reaction to virus infection.

Animals↗
PubMed1978

Alteration of islet cell populations in spontaneously diabetic mice.

Endocrine-cell populations in the islets of Langerhans of mutant mice with a severe hypoinsulinemic diabetes (ob/ob or db/db on the C57BL/KsJ background) or with a mild hyperinsulinemic diabetes (ob/ob or db/db on the C57BL/6J background) were studied quantitatively by immunofluorescence and morphometry. In severely diabetic mice, islets presented a reduced proportion of insulin containing cells but increased glucagon-, somatostatin-, and pancreatic polypeptide (PP)-containing cells, as compared with islets of control (+/+) mice. An inverse change was observed in islets of mildly diabetic mice: islets were hypertrophic and composed mostly of insulin-containing cells, with decreased proportions of glucagon-, somatostatin-, and PP-containing cells. In both types of diabetic syndromes, the changes in cell populations induced a qualitative alteration of cellular interrelationships in the affected islets.

Animals↗