Plasma retinol level

Ah-responsive and Ah-nonresponsive strains females, age 10 weeks given single ip injection of 50 mg/kg BW killed after 7 days Both groups had increased body weight, increased blood EROD activity, decreased plasma retinol levels, and increased plasma total thyroid hormone levels. The Ah-responsive group also had increased hepatic pentoxyresorufin-O-deethylase activity, increased livercytochrome P-450 activity, and increased liver weight 12... 

Recently we published data that even in countries with excellent food sources and availability, insufficient vitamin A supply will occur (Schulz et ah, 2007). The aim of this trial was to analyze vitamin A and p-carotene status and investigate the contribution of nutrition to vitamin A and p-carotene supply in mother-infant pairs of multiparous births or births within short birth rates. Twenty-nine volimteers aged between 21 and 36 years were evaluated for 48 hours after delivery. In order to establish overall supply, retinol and p-carotene were determined in maternal plasma, cord blood, and colostrum via HPLC analysis. A food frequency protocol was obtained from all participants. Regardless of the high-to-moderate socioeconomic background, 27.6% of participants showed plasma retinol levels below 1.4 pmol/liter, which can be taken as borderline deficiency. In addition, 46.4% showed retinol intake <66% of RDA and 50.0% did not consume liver at all, although liver contributes as a main source for preformed retinol. Despite a high total carotenoid intake of 6.9 3.9mg/day, 20.7% of mothers showed plasma levels <0.5 pmol/liter p-carotene. 

To look at the determinants of vitamin A disposal rate, we used multiple regression analysis to relate our data on disposal rate for 62 rats to vitamin A intake, liver vitamin A levels, and plasma retinol pool size (Fig. 10) (Kelley et al., 1994). These three variables predict 91% of the variation in disposal rate 68% of the reduction in sum of squares comes from plasma retinol, 18% from liver vitamin A, and 14% from vitamin A intake. Our data indicate that disposal rate does not fall until liver vitamin A levels are essentially depleted. That is, as long as plasma retinol levels are normal, degradation rate is high, implying a nonfunctional utilization of the vitamin. We call this degradative preservation. We conclude that plasma retinol is the major determinant of vitamin A disposal rate and hypothesize that... 

Adrenocortical hormones increase the rate of hepatic mobilization of vitamin A in animals, resulting in increased plasma retinol levels. (McGillivray, 1961 Stoewsand and Scott, 1964) A similar response to ACTH or cortisone is reported to occur in children with rheumatic fever as long as the treatment continues (Wang etal, 1954). In vitro studies reported by Borek etal. (1981) using rat hepatoma cells provide evidence for the mechanism by which this interaction occurs. They showed that corticosterone and cortisol induced a two- to threefold increased net... 

Formelli F, Carsana R, Costa A, Buranelli F, Campa T, Dossena G, Magni A, Pizzichetta M (1989) Plasma retinol level reduction by the synthetic retinoid fentretinide a one year follow-up study of breast cancer patients. Cancer Res 49 6149-6152... 

Formelli F, Carsana R, Costa A (1987) N-(4-hydroxyphenyl)retinamide (4-HPR) lowers plasma retinol levels in rats. Med Sci Res 15 843-844... 

When liver vitamin A reserves fall below about 20-30 pg retinol g liver, the secretion of holo-RBP is compromised due to inadequate retinol. Plasma retinol levels begin to fall and, if liver vitamin A continues to decline, plasma levels will fall into the deficient range and will be inadequate to supply retinol to tissues. Essentially all of the vitamin A in liver can be mobilized when it is needed to meet the needs of peripheral tissues. But ultimately, vitamin A intake must increase to bring plasma retinol levels back to the normal range. 

Physiological studies have shown that the placental transfer of vitamin A is limited in most mammals. Thus, it is normal for the liver and plasma vitamin A levels of newborns to be much lower than those in adults. In humans, premature infants often have lower plasma retinol levels than full-term infants. The period of breastfeeding is important for the accrual of vitamin A reserves as shown by... 

Repeatedly it was shown that the semm retinol level and RBP level in prematures are significantly lower than that of neonates (Shah and Rajalekshmi, 1984). In the liver of prematures, significantly lower retinol levels can be foimd in comparison to neonates (Shensi et ah, 1985). Plasma values lower than 20 gg/dl are not rare in this case and they should be taken as an indicator of a relative vitamin A deficit. But a moderate vitamin A deficiency is not only a problem of countries with poor or inadequate food sources. 

There are also changes in the binding proteins in plasma as a result of the disease process. Since serum albumin falls in association with any acute iUness, this inevitably leads to a fall in plasma zinc concentration. Similarly a reduction in retinol-binding-protein concentration as part of the APR or protein malnutrition also leads to a fall in serum retinol levels, whatever the amount of retinol stores within the liver. 

A second liver retinol (retinyl ester) compartment was added to the model for reasons analogous to those for adding a second liver /3-carotene compartment. The experimental observations show an initial rise and fall in plasma retinol-d4 concentration, then a sustained plasma retinol-d4 level for —16 days after ingesting /3-carotene-dg (Fig. 4). Prior to adding the second liver retinol compartment, the model predicted that almost all... 

The predicted chylomicron retinyl-d4 ester curve is characterized by a sharp peak similar to that of the /3-carotene-dg, again in accord with the expected rapid clearance of chylomicrons foUowing a meal. The predicted plasma retinol-binding protein-retinol-d4 curve shows an initial rise and fall, then a sustained level of retinol-d4 after the /3-carotene-dg dose. This is very similar in shape to that seen when the same subject ingested retinyl-d4 acetate in a previous experiment (Song et oL, 1995). The sustained level of retinol-d4 is a result of the slow release of retinoid into the plasma from... 

Bobbert, P, Weithauser, A., Andres, J. et al. 2009. Increased plasma retinol binding protein 4 levels in patients with inflammatory cardiomyopathy. Eur J Heart Fail 11 1163-1168. Broch, M., Gomez, J. M., Auguet, M. T. et al. 2010. Association of retinol-binding protein-4 (RBP4) with lipid parameters in obese women. Obes Surg 20 1258-1264. 

Makino, S., Fujiwara, M., Suzukawa, K. et al. 2009. Visceral obesity is associated with the metabolic syndrome and elevated plasma retinol-binding protein-4 level in obstructive sleep apnea syndrome. Horm Metab Res 41 221-226. 

Zinc deficiency accompanied by a depression in plasma retinol has been noted in several studies. Some investigators have reported an increased liver vitamin A in several species of zinc-deficient animals (Stevenson and Earle, 1956 Saraswat and Arora, 1972 J. C. Smith et aL, 1973, 1976 Brown et aL, 1976 Jacobs et al., 1978 Carney et aL, 1976). There are also reports in humans in an association between lowered zinc, retinol, and RBP (Jacobs et a/., 1978 Solomons and Russell, 1980). J. C. Smith et al, (1973) suggested that hepatic mobilization of vitamin A was impaired by zinc deficiency and their follow-up studies demonstrated a depression in liver and plasma RBP in the zinc-deficient rat compared to pair-fed controls (Brown et al., 1976 Smith et al., 1974). The depression was hypothesized to be the result of a depressed synthesis rather than an increased turnover of RBP. That preformed RBP is present in zinc-deficient rats was demonstrated by Carney et al. (1976) using labeled vitamin A. Zinc-deficient rats, whether or not they were also vitamin A-deficient, were able to mobilize over a short time span a small oral dose of vitamin A as well as could their pair-fed controls. Those animals deficient only in zinc excreted metabolites of the labeled vitamin in a similar quantitative manner as the pair-fed controls for 6 days postdosing. These data suggest that the release of retinol from retinyl ester stores, as well as a depressed RBP synthetic rate, contributed to low plasma levels of vitamin A in zinc deficiency. 

Among humans, zinc supplementation of children with protein-energy malnutrition (PEM) was reported not to alter the response in vitamin A and RBP levels immediately following admission to a hospital, but was necessary to sustain higher plasma levels throughout the recovery period. Studies in children with cystic fibrosis and in normal adult humans with moderately depressed or adequate serum zinc levels failed to demonstrate a plasma retinol response to zinc supplementation (Palin et aL, 1979 Garry and Visconti, 1980). 

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