Further observations on the teratogenic nature of insulin and its modification by supplementary treatment

Landauer, Walter; Rhodes, M. B.

doi:10.1002/jez.1401190204

Cited by 52 publications

(8 citation statements)

References 27 publications

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“…Some of these are: insulin (Landauer and Rhodes, 1952); pilocarpine (Landauer, 1953); azaserine (Dagg and Karnofsky, 1955); 5-fluorosubstituted pyrimidines (Karnofsky et al, 1958); deoxyribosyl derivatives of physiological purines Lacon, 1961, 1966); acetazolamide and N-ethylnicotinamide (Landauer and Wakasugi, 1967); cortisone (Moscona and Karnofsky, 1960); cooling of eggs during incubation (Ancel, 1958(Ancel, , 1959; and hypoxia during incubation (Grabowski and Paar, 1958). Some of these are: insulin (Landauer and Rhodes, 1952); pilocarpine (Landauer, 1953); azaserine (Dagg and Karnofsky, 1955); 5-fluorosubstituted pyrimidines (Karnofsky et al, 1958); deoxyribosyl derivatives of physiological purines Lacon, 1961, 1966); acetazolamide and N-ethylnicotinamide (Landauer and Wakasugi, 1967); cortisone (Moscona and Karnofsky, 1960); cooling of eggs during incubation (Ancel, 1958(Ancel, , 1959; and hypoxia during incubation (Grabowski and Paar, 1958).…”

Section: Introductionmentioning

confidence: 99%

Genetics of Cleft Palate in Chickens and the Relationship Between the Occurrence of the Trait and Maternal Riboflavin Deficiency

Juriloff

Roberts

1975

Poultry Science

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Reciprocal crosses were made between a New Hampshire line of chickens free of cleft palate and affected individuals of a highly inbred S.C.W. Leghorn line having 30 to 50% incidence of cleft palate. The frequency of cleft palate was observed under normal and riboflavin deficient maternal nutrition for the reciprocals of the F1, F2, and backcross to the cleft palate line. Two cases of cleft palate were found in dead embryos of 1368 F1 observations. These may not have represented the genetic trait under study. The response of egg hatchability to riboflavin deficiency was shown to be earlier for cleft palate line hens than for F1 hens, but no maternal effects were found for cleft palate incidence. The frequency of cleft palate in the F2 increased from 0.7% during normal maternal nutrition, to 4.4% during maternal riboflavin deficiency. A similar increase from 8.0% to 12.4% was seen in the backcross progeny. The cleft palate trait was found to be semi-lethal, with mortality associated with severe expression of the trait. No significant sex differences in cleft palate incidence was found in the F2 or backcross generations. The F2 and backcross cleft palate data fit models of genetic control by 3 recessive loci during normal maternal nutrition, and 2 recessive loci during maternal riboflavin deficiency. Penetrance was indicated to be under additive genetic control, and the average was calculated to be between 50 and 75% for all cases. The loss of relevance of one locus during maternal riboflavin deficiency was interpreted to indicate that the homozygous recessive condition at that locus gave disturbed riboflavin metabolism. It was further interpreted to explain the increased occurrence of some traits during teratogenic circumstances as due to the increased probability of obtaining recessive homozygosity at (n - 1) loci compared to (n) loci, and that the role of teratogens in some traits may be in mimicking specific genetic components of the traits.

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Section: Introductionmentioning

confidence: 99%

Genetics of Cleft Palate in Chickens and the Relationship Between the Occurrence of the Trait and Maternal Riboflavin Deficiency

Juriloff

Roberts

1975

Poultry Science

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“…Insulin, injected in large amounts into the chicken egg induces teratogenetic changes in the developing chick embryo, i.e., mainly skeletal and brain malformations (Landauer, 1947;Landauer and Rhodes, 1952;Barron and MacKenzie, 1962;Hickey and Klein, 1966). However, endogenous insulin is present in the egg before and after fertilization, and in the embryo itself from the second day of development (De Pablo et al, 1982).…”

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Transient stimulation of glucose metabolism by insulin in the 1‐day chick embryo

Baroffio

Raddatz

Markert

et al. 1986

Journal Cellular Physiology

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Effects of insulin upon glucose metabolism were investigated in chick embryos explanted in vitro during the first 30 h of incubation. Insulin stimulated the glucose consumption of the chick gastrula (18 h) and neurula (24 h), but had no effect on the late blastula (0 h:laying) and on the stage of six to eight somites (30 h). The increase in glucose consumption concerned both the embryonic area pellucida (AP) and extraembryonic area opaca (AO). AP responded to a greater extent (50%) and at a lower range of concentrations (0.1-1.0 ng/ml) than AO (30%; 1-100 ng/ml). Insulin had no effect on the oxygen consumption of blastoderms, whereas it stimulated the aerobic lactate production (approximately 70% of the additional glucose consumption was converted to lactate). The nanomolar range of stimulating concentrations suggests that insulin has a specific effect in the chick embryo, and that it could modulate glucose metabolism in ovo as well. The transient sensitivity of the embryo to insulin is discussed in relation to behavior of mesodermal cells.

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“…Insulin is known to cause teratogenic changes in chick embryos during the first 2 days of incubation (Laudauer, 1947;Landauer and Rhodes, 1952;Hickey and Klein, 1966) and to alter DNA, RNA, and protein content (Hickey and Klein, 1966). In cultured cells, plasmalemmal micropappendages increase upon exposure to insulin (Evans et al, 1974).…”

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The effect of insulin‐glucose on microappendages of the plasmalemma in the early chick embryo

Highison

Low

1981

Am. J. Anat.

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Chick embryos incubated for 18-24 hours (stages 4-6) were immersed for 3-5 minutes in Hanks' Balanced Salt Solution containing either insulin (10(-9) M) or D-glucose (10(-1) M) or a mixture of both. The ventral and dorsal surfaces of the entoderm and the ventral aspect of the mesoblast were examined in a scanning electron microscope. D-glucose alone or insulin alone produced negligible change. When combined these ingredients generated highly pleomorphic microappendages of the plasmalemma. The ventral surface of the entoderm was characterized by a large number of microvilli, both long and short. Concentrations of microvilli and blebs appeared in recesses at cell margins. Some of these represented mesoblastic protrusions through intercellular apertures in the entoderm. The dorsal entodermal surface developed stellate clusters of microvilli and blebs. The ventral aspect of the mesoblast became the most pleomorphic area of all. It possessed a variety of microappendages including large populations of microvilli and blebs that resembled the protrusions observed from the subblastodermic cavity. There were also stellate clusters similar to those on the dorsal entodermal surface. The same mesoblastic area in controls was virtually free of microappendages. The mesoblastic protrusions, occurring as they do prior to an established circulation, are interpreted as a "feeding" phenomenon.

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Further observations on the teratogenic nature of insulin and its modification by supplementary treatment

Cited by 52 publications

References 27 publications

Genetics of Cleft Palate in Chickens and the Relationship Between the Occurrence of the Trait and Maternal Riboflavin Deficiency

Genetics of Cleft Palate in Chickens and the Relationship Between the Occurrence of the Trait and Maternal Riboflavin Deficiency

Transient stimulation of glucose metabolism by insulin in the 1‐day chick embryo

The effect of insulin‐glucose on microappendages of the plasmalemma in the early chick embryo

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