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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

Systemic and colonic measures of inflammation. (a) KC increased following carrageenan, both alone and in combination with HFD after 50 weeks of exposure (P < 0.001; n = 27). (b) Fecal calprotectin increased in carrageenan alone and in HFD + carrageenan (P < 0.001, n = 27), but not in HFD alone. (c) Serum IL-6 and MCP-1 were significantly increased following carrageenan and HFD + carrageenan, compared to control and HFD alone in adipose tissue (P < 0.001), muscle (P < 0.01), and liver (P < 0.001; n = 3 per group). IL-10 was significantly increased following HFD and HFD + carrageenan (P < 0.05; one-way ANOVA with Tukey-Kramer posttest; n = 3 per group). HFD = high fat diet; CGN = carrageenan; KC = keratinocyte-derived chemokine.
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fig6: Systemic and colonic measures of inflammation. (a) KC increased following carrageenan, both alone and in combination with HFD after 50 weeks of exposure (P < 0.001; n = 27). (b) Fecal calprotectin increased in carrageenan alone and in HFD + carrageenan (P < 0.001, n = 27), but not in HFD alone. (c) Serum IL-6 and MCP-1 were significantly increased following carrageenan and HFD + carrageenan, compared to control and HFD alone in adipose tissue (P < 0.001), muscle (P < 0.01), and liver (P < 0.001; n = 3 per group). IL-10 was significantly increased following HFD and HFD + carrageenan (P < 0.05; one-way ANOVA with Tukey-Kramer posttest; n = 3 per group). HFD = high fat diet; CGN = carrageenan; KC = keratinocyte-derived chemokine.

Mentions: In the carrageenan-exposed mice (both carrageenan alone and HFD + carrageenan), keratinocyte-derived chemokine (KC), the murine homolog of interleukin-8, was increased from control level of 97.4 ± 10.1 ng/L to 214.6 ± 12.4 ng/L and 220.4 ± 15.6 ng/L, respectively, (P < 0.001) at 50 weeks (Figure 6(a)). In the HFD only mice, the KC value was unchanged. Similarly, fecal calprotectin was increased at 50 weeks in the carrageenan alone and HFD + carrageenan groups (P < 0.001), but not in the HFD alone group (Figure 6(b)). Measurements of other cytokines demonstrated that IL-6 and MCP-1 were significantly increased following carrageenan and HFD + carrageenan, compared to control and HFD alone (P < 0.001, P < 0.001) (Figure 6(c)). IL-10 was increased by HFD and HFD + carrageenan, compared to control and carrageenan alone (P < 0.05, P < 0.05). No differences were evident in serum TNF-α, leptin, or IL-1β. Table 1 shows differences in mRNA expression of IL-6, MCP-1, and TNF-α in adipose, muscle, and liver tissue following carrageenan, HFD, or HFD + carrageenan by QRT-PCR. Results showed significant increases (P < 0.001) in IL-6 and MCP-1 expression following carrageenan and HFD + carrageenan in adipose, muscle, and liver tissue. TNF-α expression was significantly increased following HFD and HFD + carrageenan in adipose and liver tissues and in liver tissue following carrageenan alone.


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)

Systemic and colonic measures of inflammation. (a) KC increased following carrageenan, both alone and in combination with HFD after 50 weeks of exposure (P < 0.001; n = 27). (b) Fecal calprotectin increased in carrageenan alone and in HFD + carrageenan (P < 0.001, n = 27), but not in HFD alone. (c) Serum IL-6 and MCP-1 were significantly increased following carrageenan and HFD + carrageenan, compared to control and HFD alone in adipose tissue (P < 0.001), muscle (P < 0.01), and liver (P < 0.001; n = 3 per group). IL-10 was significantly increased following HFD and HFD + carrageenan (P < 0.05; one-way ANOVA with Tukey-Kramer posttest; n = 3 per group). HFD = high fat diet; CGN = carrageenan; KC = keratinocyte-derived chemokine.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4390184&req=5

fig6: Systemic and colonic measures of inflammation. (a) KC increased following carrageenan, both alone and in combination with HFD after 50 weeks of exposure (P < 0.001; n = 27). (b) Fecal calprotectin increased in carrageenan alone and in HFD + carrageenan (P < 0.001, n = 27), but not in HFD alone. (c) Serum IL-6 and MCP-1 were significantly increased following carrageenan and HFD + carrageenan, compared to control and HFD alone in adipose tissue (P < 0.001), muscle (P < 0.01), and liver (P < 0.001; n = 3 per group). IL-10 was significantly increased following HFD and HFD + carrageenan (P < 0.05; one-way ANOVA with Tukey-Kramer posttest; n = 3 per group). HFD = high fat diet; CGN = carrageenan; KC = keratinocyte-derived chemokine.
Mentions: In the carrageenan-exposed mice (both carrageenan alone and HFD + carrageenan), keratinocyte-derived chemokine (KC), the murine homolog of interleukin-8, was increased from control level of 97.4 ± 10.1 ng/L to 214.6 ± 12.4 ng/L and 220.4 ± 15.6 ng/L, respectively, (P < 0.001) at 50 weeks (Figure 6(a)). In the HFD only mice, the KC value was unchanged. Similarly, fecal calprotectin was increased at 50 weeks in the carrageenan alone and HFD + carrageenan groups (P < 0.001), but not in the HFD alone group (Figure 6(b)). Measurements of other cytokines demonstrated that IL-6 and MCP-1 were significantly increased following carrageenan and HFD + carrageenan, compared to control and HFD alone (P < 0.001, P < 0.001) (Figure 6(c)). IL-10 was increased by HFD and HFD + carrageenan, compared to control and carrageenan alone (P < 0.05, P < 0.05). No differences were evident in serum TNF-α, leptin, or IL-1β. Table 1 shows differences in mRNA expression of IL-6, MCP-1, and TNF-α in adipose, muscle, and liver tissue following carrageenan, HFD, or HFD + carrageenan by QRT-PCR. Results showed significant increases (P < 0.001) in IL-6 and MCP-1 expression following carrageenan and HFD + carrageenan in adipose, muscle, and liver tissue. TNF-α expression was significantly increased following HFD and HFD + carrageenan in adipose and liver tissues and in liver tissue following carrageenan alone.

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