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Biomedical subjects

M Westberg

Publications and source records attributed to M Westberg.

9 recordsLinked to original sources
PubMed2001

Social dominance rank and accessory sex glands in wild adult male house mice born to food-deprived mothers.

Food deprivation after weaning often has greater effects on the reproduction of females than males. However, if animals are deprived prenatally (i.e., through deprivation of the mother during gestation), the reproduction of males may be more negatively impacted because it may decrease their ability to compete with other males and their attractiveness to females. We tested the predictions that adult sons of females that are food-deprived during gestation would tend to lose agonistic encounters with sons of well-nourished (control) females and would have smaller accessory sex glands as well. Sons of control mothers were more frequently dominant to sons of deprived mothers. They also had heavier vesicular-coagulating gland complexes and tended to have heavier preputial glands. However, among males that had not been tested for social dominance rank, there were no such differences in accessory gland weights. These data indicate that maternal food deprivation affects sons only if they engage in agonistic encounters. These effects may be due to a disruption of the organizational effects of testosterone that occur in neonatal male mice and they are likely to have a strong negative impact on the reproduction of the sons of deprived mothers.

Animals↗
PubMed2001

Maternal nutrition and reproduction of daughters in wild house mice (Mus musculus).

Food deprivation after weaning often has greater effects on the reproductive success of females than of males. However, if animals are deprived prenatally (that is, through food deprivation of the mother during gestation), the reproductive success of males may be more adversely affected than that of females because of a disruption in the organizational effects of testosterone in neonatal male mice. The hypotheses that daughters of female mice deprived of food during gestation would have lower reproductive success than control daughters, but that the impact of maternal food deprivation would be lower for daughters than it would be for sons, was tested. There was no difference in the proportion of daughters of food-deprived and control mothers that produced one or two litters. However, the mean number of pups weaned in the second litters by daughters of control females (5.9 +/- 0.57 SEM) was greater than the number of pups weaned by daughters of food-deprived females (4.5 +/- 0.65 SEM). There were no differences in the mean birth or weaning body weights of offspring. Therefore, maternal food deprivation in mice may have a small but significant effect on the reproductive success of daughters. However, studies of sons born to females that were subjected to the same food deprivation protocol indicate that maternal food deprivation may have a much greater effect on the reproduction of sons than on that of daughters.

Animals↗
PubMed1988

Low-molecular-mass surfactant protein type 1. The primary structure of a hydrophobic 8-kDa polypeptide with eight half-cystine residues.

The low-molecular-mass surfactant protein fraction, soluble in chloroform/methanol, contains at least two separate polypeptide chains. The 8-kDa form (type I) was isolated, [14C]carboxymethylated after reduction, and submitted to structural analysis. Its highly hydrophobic nature complicated purification, proteolytic cleavages, and sequence analysis. Acid hydrolysis in 6 M HCl for 7 days was necessary for release of branched-chain residues in full yield. Pepsin was the only enzyme found to cleave the surfactant protein and was used to complement peptide generation by chemical cleavage with CNBr. The primary structure deduced consists of 79 residues with 8 half-cystine residues, and a total of 39% branched-chain hydrophobic residues. However, 11 residues are charged at physiological pH, and all properties of the primary structure are not entirely outstanding in relation to those of other proteins. Hydrophobic segments, coupled with a presumably tight folding from the presence of disulfide bridges, probably explain the unusual properties and the solubility in organic solvents.

Amino Acid Sequence↗
PubMed1988

The priming effect of glucose on insulin release does not involve redistribution of secretory granules within the pancreatic B-cell.

Short-term stimulation of the pancreatic B-cell with glucose produces a time-dependent potentiation of this cell, which markedly enhances the insulin response to a renewed stimulation with the hexose. To study if a redistribution of the B-cell secretory granules to a location close to the B-cell plasma membrane could underlie the priming effect of glucose, an investigation by ultrastructural morphometry was performed. After exposure of perfused rat pancreas to non-priming or priming concentrations of glucose, pale and dark B-cell secretory granules were distinguished and analysed both within a central and a peripheral zone of the B-cell. The pale secretory granules comprised 30-40% of the total granule population in the B-cell. Whereas no difference in diameter of the granules was observed, there was evidence for a greater numerical density of dark granules in the central than in the peripheral part of the B-cell. This finding may be in line with observations implying that newly synthesized insulin is released preferentially to older insulin. The present experiments did, however, not reveal any significant priming effect of glucose on the intracellular distribution of secretory granules in the pancreatic B-cell. The lack of morphological changes in the B-cell by glucose priming of insulin release should, rather, direct increased attention to the biochemical aspects of the priming phenomenon.

Animals↗
PubMed1987

B cell insensitivity in a rat model of non-insulin-dependent diabetes. Evidence for a rapidly reversible effect of previous hyperglycemia.

In perfused pancreas of rats rendered diabetic by streptozotocin injection (STZ) during neonatal age the insulin response to 27 mM glucose was significant but impaired. It was unaffected by the alpha adrenergic blocker phentolamine. When 27 mM mannoheptulose was added simultaneously with 27 mM glucose, insulin release was inhibited, but less promptly than in pancreases from non-diabetic rats. When mannoheptulose was introduced 15 min after starting perfusion with 27 mM glucose, inhibition was apparent in non-diabetic rats, but not in STZ. In non-diabetic rats perfusion without glucose for 40 min failed to affect the subsequent response to 27 mM glucose. Conversely, in STZ, glucose omission enhanced 3.7-fold the response to 27 mM glucose. Insulin release in response to 3-isobutyl-1-methylxanthine (IBMX) was more marked in STZ than in non-diabetic rats. After glucose omission the IBMX-induced response was, however, reduced (67%) in STZ, but not significantly (7%) in non-diabetic rats. Thus, glucopenia in vitro sensitizes B cells of STZ to glucose, but desensitizes them to IBMX. Abnormal responsiveness may be linked to metabolic consequences of B cell fuel abundance.

1-Methyl-3-isobutylxanthine↗
PubMed1987

Abnormal B-cell function in neonatally streptozotocin-diabetic rats: insensitivity to alloxan toxicity.

The apparent toxicity of alloxan was compared in nondiabetic rats and rats made diabetic by injection with streptozotocin during neonatal life (STZ). In the perfused pancreas of nondiabetic rats, 1 mM alloxan rapidly but evanescently stimulated insulin secretion; this effect was followed by pronounced inhibition of the insulin response to 27 mM glucose (94% inhibition) or 1 mM 3-isobutyl-1-methylxanthine (76% inhibition). Conversely, in STZ-diabetic rats the stimulatory effect of alloxan was reduced to 22% of that elicited in nondiabetic rats. In further contrast, the inhibitory effect of alloxan exposure was abolished with regard to subsequent glucose-induced insulin secretion and attenuated with regard to 3-isobutyl-1-methylxanthine-induced insulin secretion. A relative insensitivity to alloxan was also seen in collagenase-isolated islets, where alloxan completely abolished glucose-induced insulin secretion in islets from nondiabetic rats, but only nonsignificantly reduced secretion (by 37%) in islets from STZ-diabetic rats. Insensitivity to glucose in STZ diabetic rats is associated with insensitivity to alloxan. This implies a common defect in the initial recognition site of glucose and alloxan.

1-Methyl-3-isobutylxanthine↗