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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

Hyperinsulinemic-euglycemic studies after 18 days of carrageenan exposure. (a) Blood glucose (mg/dL) was higher in the carrageenan-exposed mice than in the control mice at t = 20 minutes. Elevation occurred when the glucose infusion rates were similar (see (b)) (n per group = 10). (b) Glucose infusion rate (mg/kg/minute) was significantly less in the carrageenan-exposed mice than in the control mice from 30 to 50 minutes, and the interval to achieve steady-state was prolonged by 30 minutes. (c) Endogenous Ra was significantly less at baseline in the carrageenan-exposed mice than in the control mice. At steady-state, values were similar. (d) Rd, rate of disappearance of glucose, was significantly less following carrageenan exposure at baseline, but similar at steady-state. (e) Serum insulin levels were similar before and after infusion (N.D. = no difference).
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fig2: Hyperinsulinemic-euglycemic studies after 18 days of carrageenan exposure. (a) Blood glucose (mg/dL) was higher in the carrageenan-exposed mice than in the control mice at t = 20 minutes. Elevation occurred when the glucose infusion rates were similar (see (b)) (n per group = 10). (b) Glucose infusion rate (mg/kg/minute) was significantly less in the carrageenan-exposed mice than in the control mice from 30 to 50 minutes, and the interval to achieve steady-state was prolonged by 30 minutes. (c) Endogenous Ra was significantly less at baseline in the carrageenan-exposed mice than in the control mice. At steady-state, values were similar. (d) Rd, rate of disappearance of glucose, was significantly less following carrageenan exposure at baseline, but similar at steady-state. (e) Serum insulin levels were similar before and after infusion (N.D. = no difference).

Mentions: Hyperinsulinemic-euglycemic clamp studies were performed at the Mouse Metabolic Phenotyping Center (MMPC) at Vanderbilt University after carrageenan ingestion for 18 days. At 20 minutes, glucose levels were significantly higher in the carrageenan-exposed mice (Figure 2(a)), although glucose infusion rates were identical (Figure 2(b)). The rise in glucose levels upon initiation of the infusions was steeper in the carrageenan-exposed animals than in the controls. Subsequently, the glucose infusion rate required to maintain euglycemia was less in the carrageenan-exposed mice from t = 30 minutes to t = 90 minutes (Figure 2(b)). Steady-state was achieved 30 minutes later, from 70 minutes in the control mice to 100 minutes in the carrageenan-exposed mice, consistent with insulin resistance in the nonsteady-state. At steady-state, when the maximal effects of hyperinsulinemia were present, hepatic glucose production was fully suppressed (Figure 2(c)) and glucose disappearance rates were similar in control and carrageenan-treated mice (Figure 2(d)). Plasma insulin levels were similar at baseline and at steady-state between the carrageenan-exposed and control mice (Figure 2(e)). The uptake of 14C-2-deoxyglucose, which was infused at 120 minutes, was not significantly greater at any site (Table 2). Overall, findings demonstrate reduced baseline hepatic glucose production, impaired insulin sensitivity with lower rate of glucose infusion to achieve euglycemia, and suppression of endogenous hepatic glucose production in response to hyperinsulinemia in the steady-state.


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)

Hyperinsulinemic-euglycemic studies after 18 days of carrageenan exposure. (a) Blood glucose (mg/dL) was higher in the carrageenan-exposed mice than in the control mice at t = 20 minutes. Elevation occurred when the glucose infusion rates were similar (see (b)) (n per group = 10). (b) Glucose infusion rate (mg/kg/minute) was significantly less in the carrageenan-exposed mice than in the control mice from 30 to 50 minutes, and the interval to achieve steady-state was prolonged by 30 minutes. (c) Endogenous Ra was significantly less at baseline in the carrageenan-exposed mice than in the control mice. At steady-state, values were similar. (d) Rd, rate of disappearance of glucose, was significantly less following carrageenan exposure at baseline, but similar at steady-state. (e) Serum insulin levels were similar before and after infusion (N.D. = no difference).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig2: Hyperinsulinemic-euglycemic studies after 18 days of carrageenan exposure. (a) Blood glucose (mg/dL) was higher in the carrageenan-exposed mice than in the control mice at t = 20 minutes. Elevation occurred when the glucose infusion rates were similar (see (b)) (n per group = 10). (b) Glucose infusion rate (mg/kg/minute) was significantly less in the carrageenan-exposed mice than in the control mice from 30 to 50 minutes, and the interval to achieve steady-state was prolonged by 30 minutes. (c) Endogenous Ra was significantly less at baseline in the carrageenan-exposed mice than in the control mice. At steady-state, values were similar. (d) Rd, rate of disappearance of glucose, was significantly less following carrageenan exposure at baseline, but similar at steady-state. (e) Serum insulin levels were similar before and after infusion (N.D. = no difference).
Mentions: Hyperinsulinemic-euglycemic clamp studies were performed at the Mouse Metabolic Phenotyping Center (MMPC) at Vanderbilt University after carrageenan ingestion for 18 days. At 20 minutes, glucose levels were significantly higher in the carrageenan-exposed mice (Figure 2(a)), although glucose infusion rates were identical (Figure 2(b)). The rise in glucose levels upon initiation of the infusions was steeper in the carrageenan-exposed animals than in the controls. Subsequently, the glucose infusion rate required to maintain euglycemia was less in the carrageenan-exposed mice from t = 30 minutes to t = 90 minutes (Figure 2(b)). Steady-state was achieved 30 minutes later, from 70 minutes in the control mice to 100 minutes in the carrageenan-exposed mice, consistent with insulin resistance in the nonsteady-state. At steady-state, when the maximal effects of hyperinsulinemia were present, hepatic glucose production was fully suppressed (Figure 2(c)) and glucose disappearance rates were similar in control and carrageenan-treated mice (Figure 2(d)). Plasma insulin levels were similar at baseline and at steady-state between the carrageenan-exposed and control mice (Figure 2(e)). The uptake of 14C-2-deoxyglucose, which was infused at 120 minutes, was not significantly greater at any site (Table 2). Overall, findings demonstrate reduced baseline hepatic glucose production, impaired insulin sensitivity with lower rate of glucose infusion to achieve euglycemia, and suppression of endogenous hepatic glucose production in response to hyperinsulinemia in the steady-state.

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