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Exposure to common food additive carrageenan alone leads to fasting hyperglycemia and in combination with high fat diet exacerbates glucose intolerance and hyperlipidemia without effect on weight.

Bhattacharyya S, Feferman L, Unterman T, Tobacman JK - J Diabetes Res (2015)

Bottom Line: In contrast to high fat, carrageenan did not lead to weight gain.Carrageenan in the Western diet may contribute to the development of diabetes and the effects of high fat consumption.Carrageenan may be useful as a nonobese model of diabetes in the mouse.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine, University of Illinois at Chicago, Chicago, IL 60612-4325, USA ; Jesse Brown VA Medical Center, Chicago, IL 60612-3728, USA.

ABSTRACT

Aims: Major aims were to determine whether exposure to the commonly used food additive carrageenan could induce fasting hyperglycemia and could increase the effects of a high fat diet on glucose intolerance and dyslipidemia.

Methods: C57BL/6J mice were exposed to either carrageenan, high fat diet, or the combination of high fat diet and carrageenan, or untreated, for one year. Effects on fasting blood glucose, glucose tolerance, lipid parameters, weight, glycogen stores, and inflammation were compared.

Results: Exposure to carrageenan led to glucose intolerance by six days and produced elevated fasting blood glucose by 23 weeks. Effects of carrageenan on glucose tolerance were more severe than from high fat alone. Carrageenan in combination with high fat produced earlier onset of fasting hyperglycemia and higher glucose levels in glucose tolerance tests and exacerbated dyslipidemia. In contrast to high fat, carrageenan did not lead to weight gain. In hyperinsulinemic, euglycemic clamp studies, the carrageenan-exposed mice had higher early glucose levels and lower glucose infusion rate and longer interval to achieve the steady-state.

Conclusions: Carrageenan in the Western diet may contribute to the development of diabetes and the effects of high fat consumption. Carrageenan may be useful as a nonobese model of diabetes in the mouse.

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Related in: MedlinePlus

Hepatic glycogen stores declined following carrageenan. (a) Hepatic glycogen was higher in control and HFD groups in blood samples obtained at 50 weeks (P < 0.01; n = 27). (b)–(e) Representative sections of mouse liver stained for glycogen by periodic acid Schiff (PAS) in control (b), carrageenan-exposed (c), HFD alone (d), and HFD + carrageenan-exposed (e) mice after 52 weeks showed more intense staining in control and HFD tissues. Marker = 10 μm; original magnification 100x; CGN = carrageenan; HFD = high fat diet.
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fig4: Hepatic glycogen stores declined following carrageenan. (a) Hepatic glycogen was higher in control and HFD groups in blood samples obtained at 50 weeks (P < 0.01; n = 27). (b)–(e) Representative sections of mouse liver stained for glycogen by periodic acid Schiff (PAS) in control (b), carrageenan-exposed (c), HFD alone (d), and HFD + carrageenan-exposed (e) mice after 52 weeks showed more intense staining in control and HFD tissues. Marker = 10 μm; original magnification 100x; CGN = carrageenan; HFD = high fat diet.

Mentions: Glycogen differs from carrageenan by the presence of α-1,4-galactosidic bonds, in contrast to the α-1,3-galactosidic and β-1,4-galactosidic bonds of carrageenan. When glycogen was measured in the hepatic tissue from the four groups of mice, values were significantly lower following carrageenan than in control or high fat diet alone groups (P < 0.001) (Figure 4(a)). Similarly, when hepatic sections from control, carrageenan-exposed, HFD-exposed, and HFD + carrageenan-exposed mice were stained by periodic acid Schiff reagent, intensity of staining was greater in the control (Figure 4(b)) and HFD (Figure 4(d)) groups than in the CGN (Figure 4(d)) or CGN + HFD (Figure 4(e)) group.


Exposure to common food additive carrageenan alone leads to fasting hyperglycemia and in combination with high fat diet exacerbates glucose intolerance and hyperlipidemia without effect on weight.

Bhattacharyya S, Feferman L, Unterman T, Tobacman JK - J Diabetes Res (2015)

Hepatic glycogen stores declined following carrageenan. (a) Hepatic glycogen was higher in control and HFD groups in blood samples obtained at 50 weeks (P < 0.01; n = 27). (b)–(e) Representative sections of mouse liver stained for glycogen by periodic acid Schiff (PAS) in control (b), carrageenan-exposed (c), HFD alone (d), and HFD + carrageenan-exposed (e) mice after 52 weeks showed more intense staining in control and HFD tissues. Marker = 10 μm; original magnification 100x; CGN = carrageenan; HFD = high fat diet.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4390184&req=5

fig4: Hepatic glycogen stores declined following carrageenan. (a) Hepatic glycogen was higher in control and HFD groups in blood samples obtained at 50 weeks (P < 0.01; n = 27). (b)–(e) Representative sections of mouse liver stained for glycogen by periodic acid Schiff (PAS) in control (b), carrageenan-exposed (c), HFD alone (d), and HFD + carrageenan-exposed (e) mice after 52 weeks showed more intense staining in control and HFD tissues. Marker = 10 μm; original magnification 100x; CGN = carrageenan; HFD = high fat diet.
Mentions: Glycogen differs from carrageenan by the presence of α-1,4-galactosidic bonds, in contrast to the α-1,3-galactosidic and β-1,4-galactosidic bonds of carrageenan. When glycogen was measured in the hepatic tissue from the four groups of mice, values were significantly lower following carrageenan than in control or high fat diet alone groups (P < 0.001) (Figure 4(a)). Similarly, when hepatic sections from control, carrageenan-exposed, HFD-exposed, and HFD + carrageenan-exposed mice were stained by periodic acid Schiff reagent, intensity of staining was greater in the control (Figure 4(b)) and HFD (Figure 4(d)) groups than in the CGN (Figure 4(d)) or CGN + HFD (Figure 4(e)) group.

Bottom Line: In contrast to high fat, carrageenan did not lead to weight gain.Carrageenan in the Western diet may contribute to the development of diabetes and the effects of high fat consumption.Carrageenan may be useful as a nonobese model of diabetes in the mouse.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine, University of Illinois at Chicago, Chicago, IL 60612-4325, USA ; Jesse Brown VA Medical Center, Chicago, IL 60612-3728, USA.

ABSTRACT

Aims: Major aims were to determine whether exposure to the commonly used food additive carrageenan could induce fasting hyperglycemia and could increase the effects of a high fat diet on glucose intolerance and dyslipidemia.

Methods: C57BL/6J mice were exposed to either carrageenan, high fat diet, or the combination of high fat diet and carrageenan, or untreated, for one year. Effects on fasting blood glucose, glucose tolerance, lipid parameters, weight, glycogen stores, and inflammation were compared.

Results: Exposure to carrageenan led to glucose intolerance by six days and produced elevated fasting blood glucose by 23 weeks. Effects of carrageenan on glucose tolerance were more severe than from high fat alone. Carrageenan in combination with high fat produced earlier onset of fasting hyperglycemia and higher glucose levels in glucose tolerance tests and exacerbated dyslipidemia. In contrast to high fat, carrageenan did not lead to weight gain. In hyperinsulinemic, euglycemic clamp studies, the carrageenan-exposed mice had higher early glucose levels and lower glucose infusion rate and longer interval to achieve the steady-state.

Conclusions: Carrageenan in the Western diet may contribute to the development of diabetes and the effects of high fat consumption. Carrageenan may be useful as a nonobese model of diabetes in the mouse.

Show MeSH
Related in: MedlinePlus