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The prevalence of diabetes type 2 seems to becoming more and more normal in everyday life, and several factors influence this phenomenon. Although obesity is one of the contributing factors, we look on this page how the amazing supplement called astaxanthin – made from marine algae – can assist with this. Interesting enough, the manufacturers of Astaxanthin also has a patent pending for astaxanthin and weight loss (BMI reduction).
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Other pages of interest regarding the effect of astaxanthin:
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Diabetes mellitus is a national epidemic that is critically linked to the prevalence of obesity. More than 20 million Americans have diabetes, which includes 5.2 million who remain undiagnosed. If nothing is done, this increasing trend will continue because 60 million Americans are obese (30% of the US population over 20 years old). Furthermore, almost 9 million 6-19 year olds in the US (15% of this group) are overweight.
This situation puts a heavy financial burden on the wealth of the US population because at least 132 billion US Dollars is spent annually (1997 est.) because diabetic complications may lead to blindness, kidney failure, or amputations. In addition, heart disease and stroke make up approximately 65% of death amongst diabetics making this epidemic the 6th leading killer in the US. As a result, the indirect and direct medical expenditure of diabetics represent almost 5 times that of a non-diabetic.
In most cases, diabetes is treated with medication, although about 20% of diabetics may be managed by lifestyle changes. This means that even if we cannot change the genetic influences, fortunately, for most of us diabetes is preventable; for example, making dietary changes, taking nutritional supplements and exercising. To highlight this, people in high-risk groups who achieve a 5-7% cut in body weight will reduce risk of developing diabetes approximately 58% across all age and ethic groups.
While the debate between the contributory effects of carbohydrate and fat intake continues unabated, research reveals a strong link between foods with high glycemic index and prevalence of type 2 diabetes. Excess blood glucose needs to be converted by insulin (produced by the pancreas ß-cells) into glycogen stores, however, when glycogen stores are full, glucose is converted into fat. Over time, the body’s cells may eventually become desensitized to insulin making it necessary to produce more insulin to achieve the same affect. It is this process that would eventually lead to a state known as hyperinsulinaemic state. As a result, the body looses it ability to control high blood glucose levels (hyperglycemia) that could result in toxic conditions and promote further complications such as kidney failure.
Astaxanthin displayed positive effects in a type 2 diabetic mouse model in that it reduced the disease progression by retarding glucose toxicity and kidney damage. This has profound implications for people who belong to high-risk groups, display pre-diabetic conditions (impaired fasting glucose or impaired glucose tolerance) or want to manage advanced diabetic kidney problems (nephropathy).
Studies suggested that reactive oxygen species (ROS) induced by hyperglycemia contributes to the onset of diabetic mellitus and its complications. Non-enzymatic glycosylation of proteins and mitochondria, prevalent in diabetic conditions, is a major source of ROS. For example, pancreatic ß-cells kept in high glucose concentrations show presence of advanced glycosylation products, a source of ROS, which cause the following: i) reduction of insulin expression and ii) induction of cell death (apoptosis).
ß–cells are especially vulnerable to ROS because these cells are inherently low in antioxidant status and therefore, require long-term protection. A recent study demonstrated that antioxidants (N-acetyl-L-cysteine, vitamins C and E) exerted beneficial effects in diabetic conditions such as preservation of ß-cell function, so it is likely that a more potent antioxidant such as astaxanthin can do the same or better.
Uchiyama et al., 2002 demonstrated in obese diabetes type 2 mouse model that astaxanthin preserved pancreatic ß -cell dysfunction against oxidative damage. Treated mice received 1 mg astaxanthin/day at 6 weeks of age and then tests performed at 6, 12 and 18 weeks. Observations of astaxanthin treated mice (N=8) included: i) significantly reduced fasting glucose sugar levels at 12 (P<0.01) and 18 weeks (P<0.01); and ii) decreased glucose (P<0.001) and insulin (P<0.001) levels in the blood serum. In additional, treated rats displayed better response profiles to the intraperitoneal glucose tolerance test (IPGTT at 1g glucose/kg bodyweight, Figure 1 and Figure 2).
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Figure 1. Astaxanthin improved the glucose levels in the Intraperitoneally Glucose Tolerance Test (IPGT) in diabetic mouse model. #p<0.001. Naito et al., 2002.
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This showed that astaxanthin preserved pancreas function and insulin sensitivity. Furthermore, preliminary renal damage assessment measuring urinary albumin levels revealed significantly lower glomerular (kidney) damage.
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Figure 2. Astaxanthin preserved insulin sensitivity in the diabetic mouse model. #p<0.001. Naito et al., 2002.
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This was confirmed in another study by Naito et al., 2004, who looked at diabetic nephropathy in the type 2 diabetic mouse model (Figure 3). The authors postulated that astaxanthin could also circumvent high glucose toxicity, which normally leads to increased oxidative stress and pathogenesis of kidney damage.
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Figure 3. Astaxanthin protected kidney function measured by urinary albumin protein loss. #p<0.001. Naito et al., 2004.
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As well as substantiating observations by Uchiyama et al., Naito demonstrated that astaxanthin treated type 2 diabetic mice which normally shows renal insufficiency at 16 weeks of age in fact exhibited 67% less urinary albumin loss (N=5, P<0.05) and figure 4 shows 50% less DNA damage (8-OHdG, P<0.05).
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Figure 4. Astaxanthin reduced the amount of DNA damage indicated by urinary 8-OHdG levels. #p<0.001. Naito et al., 2004.
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Furthermore, the increased protein loss was due to the vascular size ratio increase of 250% in the diabetic model. In astaxanthin treated mice, this area was significantly (P<0.05) reduced by almost 54% (Figure 5).
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Figure 5. Astaxanthin preserved the relative mensangial area. +p<0.05 vs. positive control. Naito et al., 2004.
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Although, clinical trials involving antioxidants in humans have only recently begun, these preliminary results concluded that strong antioxidant supplementation might improve type 2 diabetic control and inhibit progressive renal damage by circumventing the effects of glycation-mediated ROS under hyperglycemic conditions. Therefore, astaxanthin maybe useful as part of a therapeutic strategy against diabetes and its complications. This will be greatly assisted by the on going research of the same Japanese group based at the Kyoto Prefecture University of Medicine, who is using gene chip technology to help them understand the mechanisms at the genetic level.
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