**5. Reduction of blood triglyceride levels**

Excess lipid is stored in the form of TG in subcutaneous and internal organs in the body, and is broken down into fatty acids as required [19]. Dyslipidemia, with increased TG and Cho levels in the blood, leads to atherosclerosis, which in turn can lead to cardiovascular disease and stroke. Accumulation of TG can also result in fatty liver disease, leading to decreased hepatic function, liver cirrhosis and potential morbidity, including myocardial infarction, cerebral infarction and angina pectoris, and eventually cancer [20–23].

Since we previously observed that the TG level in blood was decreased by Ca-Alg in rats [18], we next set out to examine the effect of Ca-Alg on elevated TG levels in the blood, hepatic and total body accumulation of fat, and body weight in rats fed a TG-loaded diet for 5 weeks. We also investigated the mechanism of the TG-reducing effect of Alg in vitro [24].

Rats were randomized into five groups: a high-fat diet group (14% w/w lard, HF); 3 Ca-Alg-containing diet groups (2.5, 5 or 10% w/w Ca-Alg) and a resistant maltodextrin (RMD) diet group as a positive control (with 5% w/w RMD). The 10% Ca-Alg group showed a significant reduction of body weight increase from the 7th day. The increase of TG in blood was also significantly suppressed, and the amount of TG excreted in feces was increased. Increase of body fat mass was in the order HF > RMD > Ca-Alg 2.5% > Ca-Alg 5% > Ca-Alg 10%, while the total weight of the extracted fat tissues was significantly reduced in the RMD, 5 and 10% Ca-Alg groups. Hepatic pathology showed clear circular vacuoles apparently representing TG accumulation in the HF group, while fewer vacuoles were seen in the Ca-Alg groups.

These results suggest that Ca-Alg lowers blood TG through direct suppression of TG absorption, independently of its effect on Cho. As regards the mechanism of Ca-Alg action, hepatic pathology showed that clear circular fatty droplets presumed to represent TG accumulation were present in the HF group, but were reduced in

**Figure 5.**

*Area under the blood concentration-time curve of TG in rats after the 5-week feeding period with high-fat diet or high-fat diet containing Ca-Alg or high-fat diet containing RMD [24]. The data represent means ± S.D., n = 7. \* p < 0.05, compared with high-fat diet.*

**27**

*Pharmacological Effects and Utility as a Food Additive of Calcium Alginate*

the 10% Ca-Alg group. Interestingly, the concentrations of uric acid, allantoin and BUN in plasma were also decreased in all the Ca-Alg groups, though the mechanism

These results suggest that Ca-Alg suppresses absorption of TG, leading to reduced blood TG levels, and decreases hepatic and total body accumulation of TG, in addition to promoting excretion. These findings should help to provide a rational

Diabetics may develop serious complications such as retinopathy, nephropathy and neuropathy, in addition to myocardial infarction, cerebral infarction and so on [27, 30], even though the initial subjective symptoms may be minor. Ca-Alg is known to suppress the postprandial increase of blood glucose, and therefore may be helpful in preventing lifestyle-related diseases such as diabetes. Starch is initially decomposed to maltose in the gastrointestinal tract, mainly by α-amylase, before decomposition by α-glucosidase (maltase) to glucose. Transporters located on the cell membrane surface absorb glucose. Ca-Alg should inhibit at least one of these processes to suppress blood glucose levels since it is not absorbed from the gastrointestinal tract. We therefore chose to investigate which of these processes is inhibited by Ca-Alg, and the optimal amount and particle size of Ca-Alg in the diet required

We first examined the effect of Ca-Alg concentration on α-glucosidase activity, and observed no significant change compared to the control. On the other hand, the amount of glucose adsorbed on Ca-Alg increased with increasing initial glucose concentration until it reached saturation. The direct binding affinity of glucose for

cannot be absorbed, or that are less vulnerable to lipases [24].

basis for designing future clinical trials (**Figure 6**).

**6. Suppression of postprandial blood glucose level**

to suppress the postprandial increase of blood glucose in rats [25].

We then investigated whether Alg affects lipase activity. Na-Alg was suspended in water, and diluted as required. When this solution was added to an emulsion composed of bile acid and lecithin in the presence of lipase, no decrease of lipase activity was observed, ruling out a direct effect on lipase. On the other hand, when Na-Alg was added to an emulsion composed of TG, bile acid and lecithin, the emulsion was well maintained, and a creaming phenomenon was confirmed after 5 days. When water was added to the emulsion, it disintegrated, precipitating lecithin and releasing TG on the liquid surface. These results suggest that Alg stabilizes bile acid micelles containing TG, possibly by absorbing them and forming large micelles that

*DOI: http://dx.doi.org/10.5772/intechopen.86861*

involved is unclear (**Figure 5**).

*A possible mechanism of TG-lowering effect of Ca-Alg [24].*

**Figure 6.**

*Pharmacological Effects and Utility as a Food Additive of Calcium Alginate DOI: http://dx.doi.org/10.5772/intechopen.86861*

**Figure 6.**

*Alginates - Recent Uses of This Natural Polymer*

pectoris, and eventually cancer [20–23].

effect of Alg in vitro [24].

**5. Reduction of blood triglyceride levels**

Excess lipid is stored in the form of TG in subcutaneous and internal organs in the body, and is broken down into fatty acids as required [19]. Dyslipidemia, with increased TG and Cho levels in the blood, leads to atherosclerosis, which in turn can lead to cardiovascular disease and stroke. Accumulation of TG can also result in fatty liver disease, leading to decreased hepatic function, liver cirrhosis and potential morbidity, including myocardial infarction, cerebral infarction and angina

Since we previously observed that the TG level in blood was decreased by Ca-Alg in rats [18], we next set out to examine the effect of Ca-Alg on elevated TG levels in the blood, hepatic and total body accumulation of fat, and body weight in rats fed a TG-loaded diet for 5 weeks. We also investigated the mechanism of the TG-reducing

Rats were randomized into five groups: a high-fat diet group (14% w/w lard, HF); 3 Ca-Alg-containing diet groups (2.5, 5 or 10% w/w Ca-Alg) and a resistant maltodextrin (RMD) diet group as a positive control (with 5% w/w RMD). The 10% Ca-Alg group showed a significant reduction of body weight increase from the 7th day. The increase of TG in blood was also significantly suppressed, and the amount of TG excreted in feces was increased. Increase of body fat mass was in the order HF > RMD > Ca-Alg 2.5% > Ca-Alg 5% > Ca-Alg 10%, while the total weight of the extracted fat tissues was significantly reduced in the RMD, 5 and 10% Ca-Alg groups. Hepatic pathology showed clear circular vacuoles apparently representing TG accumulation in the HF group, while fewer vacuoles were seen in the Ca-Alg

These results suggest that Ca-Alg lowers blood TG through direct suppression of TG absorption, independently of its effect on Cho. As regards the mechanism of Ca-Alg action, hepatic pathology showed that clear circular fatty droplets presumed to represent TG accumulation were present in the HF group, but were reduced in

**26**

**Figure 5.**

groups.

*n = 7. \**

*p < 0.05, compared with high-fat diet.*

*Area under the blood concentration-time curve of TG in rats after the 5-week feeding period with high-fat diet or high-fat diet containing Ca-Alg or high-fat diet containing RMD [24]. The data represent means ± S.D.,* 

*A possible mechanism of TG-lowering effect of Ca-Alg [24].*

the 10% Ca-Alg group. Interestingly, the concentrations of uric acid, allantoin and BUN in plasma were also decreased in all the Ca-Alg groups, though the mechanism involved is unclear (**Figure 5**).

We then investigated whether Alg affects lipase activity. Na-Alg was suspended in water, and diluted as required. When this solution was added to an emulsion composed of bile acid and lecithin in the presence of lipase, no decrease of lipase activity was observed, ruling out a direct effect on lipase. On the other hand, when Na-Alg was added to an emulsion composed of TG, bile acid and lecithin, the emulsion was well maintained, and a creaming phenomenon was confirmed after 5 days. When water was added to the emulsion, it disintegrated, precipitating lecithin and releasing TG on the liquid surface. These results suggest that Alg stabilizes bile acid micelles containing TG, possibly by absorbing them and forming large micelles that cannot be absorbed, or that are less vulnerable to lipases [24].

These results suggest that Ca-Alg suppresses absorption of TG, leading to reduced blood TG levels, and decreases hepatic and total body accumulation of TG, in addition to promoting excretion. These findings should help to provide a rational basis for designing future clinical trials (**Figure 6**).
