The effect of the thyroid gland on intestinal absorption of hexoses

Levin, Roy J.; Smyth, David

doi:10.1113/jphysiol.1963.sp007294

Cited by 60 publications

(30 citation statements)

References 13 publications

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“…Thyroid hormones have a marked enterotrophic action in rat (Levin & Smyth, 1963; Levin, 1969;Wall, Middleton, Pearse & Booth, 1970). Therefore, changes in morphology could influence intestinal oxygen consumption.…”

Section: Discussionmentioning

confidence: 99%

Thyroid control of small intestinal oxygen consumption and the influence of sodium ions, oxyhen tension, glucose and anaesthesia.

Levin¹,

Syme²

1975

The Journal of Physiology

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Section: Discussionmentioning

confidence: 99%

Thyroid control of small intestinal oxygen consumption and the influence of sodium ions, oxyhen tension, glucose and anaesthesia.

Levin¹,

Syme²

1975

The Journal of Physiology

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“…Although food intake increased slightly during pregnancy, the main increase in food consumption occurred during lactation, long after hyperplasia of the gastric mucosa had been established. Moreover, while hyperplasia induced under conditions such as hypothermia (Heroux & Gridgeman, 1958), experimental lesions of the hypothalamus (Brobeck, Tepperman & Long, 1943;Mayer & Yannoni, 1956), administration of insulin or thyroid extract (McKay, Callaway & Barnes, 1940;Levin & Smyth, 1963), intermittent starvation (Holeckova & Fabry, 1959) or high-bulk feeding with agents such as alfalfa or talcum (Addis, 1932;Wierda, 1950;Friedman, 1953) produces hypertrophy of the alimentary tract in rats and mice, the increase in food intake required to achieve this effect is far greater than the modest increase in food consumption that occurs early in pregnancy.…”

Section: Discussionmentioning

confidence: 99%

Hyperplasia of the gastric mucosa during pregnancy and lactation in the rat

Crean¹,

Rumsey²

1971

The Journal of Physiology

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SUMMARY1. The growth of the gastric mucosa during pregnancy and afterwards has been studied by comparing the stomachs of rats, killed at weekly intervals after impregnation, with the stomachs of virgin rats of the same age and starting weight. The rate of growth of the gastric mucosa in both groups was determined from the changes observed in the weight of the whole stomach, the weight and surface area of the fundus, the volume (mass) of the fundic mucosa and the total parietal and total peptic cell populations.2. Hyperplasia of the gastric mucosa occurred during pregnancy and lactation, the effect being characterized by increases in the surface area and volume (mass) of the gastric mucosa, and in the total parietal and total peptic cell populations.3. The data suggest that the effect developed shortly after conception. Hyperplasia of the gastric mucosa continued throughout pregnancy and reached maximal values after the second week of lactation and waned thereafter; the maximal changes obtained for individual observations such as surface area and the total parietal and total peptic cell populations represented increases of the order of 40 % above corresponding control values.4. From the observations that were made on food intake it seemed unlikely that the hyperplasia of the gastric mucosa was due to hyperphagia. It also seemed unlikely that the effect could be accounted for by the increase that occurred in body weight during pregnancy.

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“…First: Hyperthyroid patients have been shown to have increased circulating pro-insulin than active insulin levels and had reduced C-peptide levels compared to their euthyroid counterparts, suggesting an underlying defect in the proinsulin processing [18]. Second: The hyperthyroid patients are believed to have enhanced intestinal glucose absorption due to the increased expression of intestinal membrane glucose transporters [22,23]. Third: Increased rate of gluconeogenesis and hepatic glucose output by the expression of the hepatocyte membrane GluT 2 [24].…”

Section: Discussionmentioning

confidence: 99%