Cargill launches erythritol product line under  Zerose™  brand name

New Zerose™ web site helps consumers understand erythritol’s benefits

MINNEAPOLIS – Cargill has branded its erythritol product line under a new name, Zerose™ erythritol, that clearly conveys to food manufacturers and consumers that the all-natural sweetener contains zero sugar, zero calories*, zero aftertaste and zero artificial ingredients. The brand launch includes the introduction of a new consumer education web site, www.zerosesweetener.com, designed to answer questions about erythritol and explain its benefits as a natural sugar alternative.

Formerly known as Eridex™ erythritol, Zerose™ erythritol is a bulk sweetener that tastes and functions like sugar in beverages, dairy products and confections that appeal to consumers who want to manage their weight or sugar levels or sugar intake. Like sugar, it reduces water activity in a food product, provides volume and provides the freeze point depression needed in many frozen treats.

Zerose™ erythritol tastes 60 to 70 percent as sweet as sugar, so people can reduce their sugar intake without sacrificing taste. The ingredient also is non-glycemic and non-insulemic, making it a useful sugar alternative for people on diabetic diets. In addition, Zerose™ erythritol is noncariogenic (does not promote tooth decay) and is endorsed by Toothfriendly International.**

Cargill’s application and manufacturing expertise

Cargill is in a unique position with more than a decade of experience in the use and manufacture of erythritol. “We recognized the benefits of erythritol in the 1980s and began building the manufacturing, food safety and application database that led to the eventual U.S. and EU approval and commercialization of the ingredient,” said Kathy Fortmann, polyols and dextrose global business director, Cargill Sweetness Solutions. Cargill has an extensive patent portfolio through its own patent estate and through the licensing of other intellectual property.

Zerose™ erythritol is easy for food and beverage manufacturers to use because it comes in an easy-to-ship powder form, has heat and pH stability and freeze-point depression, and gives finished products the same volume that sugar does in baked goods.

Zerose™ erythritol is unique, natural and organic

Erythritol exists naturally at low levels in many fruits and at higher levels in naturally fermented foods such as soy sauce, cheese, wine and beer. Zerose™ erythritol is produced by growing a natural culture that converts sugars and other nutrients into erythritol. This process is similar to the way yogurt is made from milk.

It is then filtered, crystallized and dried, resulting in a final product that is greater than 99 percent pure. Zerose™ erythritol is natural; the ingredient also is available in a U.S. Department of Agriculture (USDA) certified organic grade (certified by QAI International).

For more information about Cargill’s sweetness products, visit www.cargillsweetness.com.

*Zero calorie determination is based on scientific studies cited in a petition submitted to the U.S. Food and Drug Administration.

Above information provided by your local chemcial and processed food company.

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The Concentrations and Ratio of Dietary Calcium and Phosphorus Influence Development of Nephrocalcinosis in Female Rats¹  

Kevin A. Cockell², Mary R. L’Abbé and Bartholomeus Belonje

Nutrition Research Division, Food Directorate, Health Products and Food Branch, Health Canada, 2203C Banting Research Centre, Ottawa, ON, Canada K1A 0L2

http://jn.nutrition.org/cgi/content/full/132/2/252

^{This reflects  issues of calcium and mineral loss during ingestion of Erythritol}  ~ Dr. E

The rats were fed the test diets for 16 wk, with feed consumption and body weight gain measured weekly. Rats were maintained in accordance with the guidelines of the Canadian Council on Animal Care, in stainless steel wire-bottomed cages in a temperature- and humidity-controlled room with a 12-h light:dark cycle. The experiment protocol was approved by the institutional Animal Care Committee of the Health Products and Food Branch of Health Canada.

Tissue sampling and histopathology.

Rats were killed by exsanguination under isoflurane anesthesia. Kidneys were dissected out and cut in half (left kidney cut longitudinally, right kidney cut transversely). One half of each was preserved in formalin for subsequent processing and paraffin embedding following routine methods for histopathology. Adjacent 5-µm sections were cut and stained with hematoxylin and eosin (H&E) or by the von Kossa technique (10 ).

Black granular precipitates on von Kossa–stained sections were manually counted and a histochemical score was assigned according to the number of granules found in one transverse plus one longitudinal kidney section per rat. A score of 0 was given for no granules found in the sections, + for 1–25 granules, ++ for 26–75 granules, +++ for 76–150 granules and ++++ for >150 granules in the sections. The other half of each kidney was frozen at -80°C for subsequent mineral analyses.

Mineral analyses.

Samples of tissues and diets were dry ashed at 450°C using concentrated nitric acid as an oxidizing agent before analysis for Ca by flame atomic absorption spectrometry (Perkin-Elmer 5100PC, Perkin-Elmer, Norwalk, CT) (11 ) and P by a colorimetric method (12 ). Analytical standards were prepared from certified single-element stock solutions (SPEX Chemical, Metuchen, NJ). These analytical methods have been checked in multilaboratory quality control studies (13 ) and analysis of NBS Bovine Liver (1577 or 1577a, National Institute of Standards and Technology, Gaithersburg, MD) gave results within 5% of certified values.

Statistical analyses.

Growth results were analyzed by ANOVA followed by Scheffé’s test for difference of means (comparing Ca + P concentration effects, diets AIN93, 1.5x, 2.5x and 4.0x) or t test for independent samples (comparing Ca:P ratio effects, AIN93 vs. AIN76 diets), using P < 0.05 as the threshold of significance. Kidney Ca+  results were analyzed by nonparametric methods (Kruskal-Wallis ANOVA followed by Dunn’s multiple comparison or Mann-Whitney U test) due to profound heterogeneity of variances, which could not be overcome by standard transformation procedures. For Kruskal-Wallis ANOVA and Mann-Whitney U test, P < 0.05 was used as the threshold of significance. For Dunn’s multiple comparison, which was performed only where Kruskal-Wallis ANOVA achieved significance, a threshold of = 0.15 was used, yielding an experiment-wise error rate threshold for significance of 0.0125 (14 ). The association between kidney Ca or P concentration and histological score was investigated using the Spearman Rank Order correlation. Statistical analyses were conducted using Statistica for Windows, version 5.1 (StatSoft, Tulsa, OK). Results are presented as mean ± SD, with ranges also specified for kidney Ca concentrations.

 
The Ca and P concentrations of the test diets were (dry weight basis): diet AIN93, 5.4 ± 0.3 g Ca and 3.9 ± 0.3 g P/kg diet, molar ratio 1.07; diet 1.5x, 7.9 ± 0.3 g Ca and 5.4 ± 0.3 g P/kg diet, molar ratio 1.12; diet 2.5x, 12.9 ± 0.2 g Ca and 8.7 ± 0.3 g P/kg diet, molar ratio 1.14; diet 4.0x, 20.3 ± 0.3 g Ca and 13.4 ± 0.2 g P/kg diet, molar ratio 1.17; diet AIN76, 5.3 ± 0.2 g Ca and 6.2 ± 0.3 g P/kg diet, molar ratio 0.66. No significant differences in body weight gain or feed efficiency were found as a result of the dietary treatments used (results not shown).

Kidney Ca+ concentration in the group of weanling rats killed at the outset of the study was 7.53 ± 0.40 µmol/g dry kidney (range 6.90–8.18) for female rats and 7.05 ± 0.30 µmol/g dry kidney (range 6.65–7.50) for male rats. All weanling rats killed at the outset of the study had histochemical scores of zero, indicating no evidence of black precipitates on von Kossa–stained kidney sections.

Male rats showed almost no histochemical evidence of NC with any of the diets and had less kidney Ca accumulation than female rats (Table 2 ). In female rats, increased kidney Ca concentration and incidence of histochemically determined NC was found after 16 wk of feeding increasing amounts of dietary Ca and P at the optimal molar ratio (comparing diets AIN93 through 4.0x, Table 2 ), although more extensive Ca accumulation and more severe NC resulted from imbalance in dietary Ca and P intakes (comparing diet AIN93 and AIN76;Table 2 and

 
These results were supported in a categorical examination of kidney Ca+ concentration, namely, the kidney calcium score (Table 2) . For categorization of kidney calcium score in our laboratory, the "normal" level for rats is 7.50 ± 0.63 µmol Ca/g dry kidney (mean ± SD) based on historical data from several studies. This value is similar to the analyzed value for female rats killed at the outset of the present study. With increasing dietary Ca and P concentrations, a higher proportion of female rats had "elevated" kidney calcium score (>2 SD above "normal") and 1 of 8 female rats fed diet 4.0x had a kidney calcium score indicative of Nephrocalcinosis (NC), >10 times the normal level (i.e., Ca concentration >75 µmol/g dry kidney). Kidney P concentration was significantly increased only in female rats fed diet AIN76 in comparison to AIN93 (445 ± 80 vs. 351 ± 11 µmol P/g dry kidney, respectively).

The location of mineral precipitation in kidney sections, shown by von Kossa staining, was similar with elevated concentrations of Ca and P at the optimal ratio (e.g., diet 4.0x, Fig. 1 B) to that seen with Ca:P imbalance (diet AIN76, Fig. 1 C) although the degree of precipitation was generally more severe in the latter group.

Most of the female rats fed diet AIN93 had no histochemical evidence of mineral precipitation after 16 wk of feeding (Fig. 1 A). There was considerable variation among rats within a treatment group in the extent of kidney Ca+ accumulation and the severity of Nephrocalcinosis (NC)    (Table 2) .

Even with diet 2.5x, there were some female rats with kidney Ca concentrations in the normal range and no histochemical evidence of NC. With diet 4.0x, all female rats showed elevated kidney Ca+, although the range of responses was still very large. Higher incidence and severity of NC was seen with the suboptimal dietary Ca:P molar ratio (diet AIN76) than when these elements were present at 4 times the normal concentrations but "optimally" balanced (diet 4.0x) (Fig. 1 and Table 2 ).   ^{This  statement  means that an imbalance of Calcium to Phosphorus accelerates Nephrocalcinosis (NC)....    ~ Dr. E}

There was a significant positive association between kidney histochemical score and kidney Ca concentration in female rats (Fig. 2 ) which yielded a Spearman Rank Order correlation coefficient r = 0.87 (P < 0.00001, n = 40). A similar positive association between kidney histochemical score and kidney P concentration in female rats (data not shown) yielded a Spearman Rank Order correlation coefficient r = 0.65 (P < 0.00001, n = 40).

 
The present study focused on the effects of elevating dietary Ca and P concentrations together while maintaining the optimal ratio of these two elements. Hoek et al. (15 ) examined the effect of increasing dietary Ca and P concentrations, comparing 0.25% Ca + 0.20% P or 0.25% Ca + 0.4% P to diets containing twice the content of each (0.5% Ca + 0.4% P or 0.5% Ca + 0.8% P, respectively). In both cases, the diets with the higher Ca + P content yielded more severe NC. Low incidence and severity of NC was found using a diet containing 0.75% Ca + 0.4% P (15 ), which is similar in Ca and P composition to our diet 1.5x.

^{This refers to blood values of dietary calcium, and its over-release  into the bloodstream, from various chemicals, diets, and other intakes or releases. Calcium may affect muscle contractility, blood vessel constriction or dilation and blood pressure, blood pressure affects kidney function, and / or other calcium-associated biological or physiological activities.}

It has been suggested that the Ca:P molar ratio must be >1 to prevent kidney calcification in female rats (16 ). Although this was achieved in our AIN93 through 4.0x diets, the higher concentrations of Ca and P intake at the recommended ratio still produced NC. Studies described by Reeves et al. (16 ) indicated that a Ca:P molar ratio of 0.97 (5 g Ca + 4 g P/kg diet) did not completely eliminate kidney calcification in female rats, although normal kidney Ca concentrations were found in female rats fed a purified diet with a Ca:P molar ratio of 1.3 for 16 wk.

The present finding of slightly elevated kidney Ca in one of eight female rats fed diet AIN93 suggests that a Ca:P molar ratio of 1.07 does not completely prevent Ca accumulation in kidneys. Earlier work in our laboratory indicated that even with a diet formulated according to AIN-93G specifications, with an analyzed Ca:P molar ratio of 1.31, some female rats had elevated kidney Ca after 16 wk of feeding, and one of eight female rats had a kidney Ca concentration consistent with Nephrocalcinosis (NC) (5 ). It is important to note that kidney Ca concentration in female rats in the present study varied widely within a treatment group, as did the severity of histochemically assessed NC. Similar results have been reported by others (2 ,5 ,15 ).

The typical histological appearance of diet-induced NC shows calcification primarily in the corticomedullary junction region (1 ) and this was the pattern seen in the present study. The von Kossa histochemical procedure detects principally phosphate and carbonate ions, which are the counterions with which Ca is commonly associated in normal and pathologically calcified tissues, rather than being specific for Ca (10 ).

Others have demonstrated that the kidney precipitates found in rats fed diets varying in Ca and/or P content, such as ours, are typically composed of calcium and phosphate (17 ,18 ). The significant association between histochemical score and kidney Ca concentration using the Spearman rank correlation indicates the robustness of this histological grading scheme. A similar correlation was shown previously in rats fed diets varying in Ca and P content (15 ,19 ,20 ) and in human renal biopsy specimens (21 ). A similar association between histochemical score and kidney P concentration has also been reported (15 ). Together, these associations support the identification of the kidney concretions found in female rats in the present study as calcium phosphate.

NC in female rats can complicate the interpretation of toxicity studies (22 –24 ). This problem has been noted in cereal-based diets as well as semipurified diets, and has led the National Toxicology Program to reformulate their standard cereal-based diet to conform to the AIN recommendation regarding Ca:P molar ratio (25 ). Because rats are one of the standard laboratory animal species used in toxicity testing for regulatory purposes (26 ), NC in rats can have widespread implications for human safety and risk assessment activities. Researchers should be cognizant of Ca and particularly P concentrations and adjust mineral mixes accordingly when substituting different protein sources in modified AIN-93G diets.

Although the reformulation leading to the AIN-93G diet was largely successful in reducing the incidence and severity of nephrocalcinosis in female rats, it must be remembered that the absolute concentrations of dietary Ca and P, and not just their ratio, influence the development of nephrocalcinosis in female rats.

 
¹ Publication no. 562 of the Bureau of Nutritional Sciences. Portions of this work were presented in poster form at the 43rd Annual Meeting of the Canadian Federation of Biological Societies, Ottawa, Canada, June 22–24, 2000 [Cockell, K. A., L’Abbé, M. R. & Belonje, B. (2000) Dietary calcium and phosphorus levels and not just their ratio, influence development of nephrocalcinosis in female rats. Abstract T156].

³ Abbreviations used: AIN93, modified AIN-93G diet containing Ca and P at the concentrations specified in the AIN-93G formulation; 1.5x, 2.5x and 4.0x, diets containing Ca and P at 1.5, 2.5 and 4.0 times, respectively, the concentrations in the AIN-93G diet; AIN76, modified AIN-93G diet containing Ca and P at the concentrations specified in the AIN-76A formulation; H&E, hematoxylin and eosin stain; NC nephrocalcinosis.

Manuscript received 6 September 2001. Initial review completed 28 September 2001. Revision accepted 27 November 2001.

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 NEW INFORMATION    Dec. 9, 2008