Green tea aids blood sugar control in mice; omega-3s prevent adipose-tissue changes that promote diabetes
by Craig Weatherby
According to the American Diabetes Association, nearly 21 million children and adults in the United States have type II diabetes: the kind caused by obesity, poor diets, and lack of exercise. And some six million of these remain dangerously unaware of their condition.
Diabetes contributed to about 224,000 deaths in 2002, and studies indicate that diabetes is generally under-reported on death certificates, particularly in the cases of older persons with multiple chronic conditions. As a consequence, the death toll attributable to diabetes may be much higher.
America’s annual bill for this lifestyle disease is estimated at $132 billion: a figure that includes lost productivity, miscellaneous medical care, and a whopping $92 billion for expensive diabetes drugs.
As we’ve reported, omega-3s from fish offer considerable promise as preventive and therapeutic agents: see “Drug May Help Prevent Diabetes but Omega-3s Offer Comparable Effects” and “Fish, omega-3s, and diabetes.”
Recent weeks witnessed the release of more promising findings on the diabetes front, regarding green tea as well as omega-3s.
High-fat diet rich in omega-3s halts pro-diabetic changes
Research published in recent years supports the idea that inflammation, obesity, and diabetes are interconnected, and highlights the fact that dietary omega-3s can discourage all three.
A new animal study from the Medical University of Vienna, Austria underscores these insidious connections and supports the hypothesis that marine omega-3s can help prevent or ameliorate type II diabetes (Todoric J et al 2006).
As Dr. Nicholas Perricone often points out, the fatty adipose tissue that accumulates around people’s waists and results in dangerous “central obesity” attracts immune-sytem cells (macrophages) that spews a steady stream of the kinds of pro-inflammatory messenger chemicals (e.g., cytokines and prostaglandins) normally generated only in response to injury, cancer, or infection.
Increases in the proportion of adipose tissue in the body also tend to reduce the “insulin sensitivity” of cells: an effect that predisposes people to developing obesity and diabetes.
As the authors of the Austrian study said, “Inflammatory alterations in white adipose tissue appear to underlie complications of obesity including diabetes mellitus."
But, as they also noted, “Polyunsaturated fatty acids… particularly those of the n-3 [omega-3] series, modulate immune responses and may ameliorate [decreases in] insulin sensitivity.”
They set tested this hypothesis by feeding fat, diabetic mice either a Low-Fat Diet or one of three diets:
- High-Fat Diet dominated by saturated and monounsaturated fatty acids.
- High-Fat Omega-6 Diet (dominated by pro-inflammatory omega-6 fatty acids).
- High-Fat Omega-3 Diet (dominated by anti-inflammatory omega-3 fatty acids from fish).
The Austrians reported that the diabetic mice on High-Fat Diet number 1 (saturated and monounsaturated fatty acids) suffered two adverse effects, compared with diabetic mice on the Low-Fat Diet:
- Increased “expression” of many pro-inflammatory genes.
- Their adipose tissue became infiltrated by immune system cells called macrophages, which release pro-inflammatory messenger chemicals.
Unsurprisingly, the mice on High-Fat Diet number 2, rich in pro-inflammatory omega-6 fatty acids, suffered similar adverse, pro-inflammatory effects in their adipose tissues.
However, the diabetic mice on the High-Fat Omega-3 Diet avoided all of the adverse, pro-inflammatory effects suffered by the other two High-Fat chow groups, despite the fact that their body weight did not drop.
In addition, while High-Fat Diets 1 and 2 reduced the animals' blood levels of adiponectin—a hormone inversely correlated with body mass index (BMI)—the levels remained desirably high in diabetic mice on the High-Fat Omega-3 Diet.
The Austrian researchers expressed the results this way (clarifying text inserted in brackets ):
“[A high-fat diet rich in omega-3s] prevent[s] adipose tissue inflammation induced by high-fat diet in obese diabetic mice… These data suggest that beneficial effects of [omega-3 fatty acids] on diabetes development could be mediated by their effect on adipose tissue inflammation.”
While not proof, these results offer more solid evidence that omega-3s may help prevent or alleviate type II diabetes in people.
Study shows green tea antioxidant’s anti-diabetic attributes
Despite its association with improved weight control, the record of green tea as an anti-diabetes agent is mixed at best, with clearly positive results reported from only one clinical trial that tested the effects of a green tea extract (Fukino Y et al 2005).
But findings published last month by researchers from Swiss manufacturer DSM Nutritional Products show that green tea extract improves glucose tolerance in diabetic mice: an effect that could help prevent type II diabetes (Wolfram S et al 2006).
We should note at the outset that these encouraging results relate to DSM’s highly concentrated green tea extract. The extract, called Teavigo™, contains unnaturally high levels (94 percent by weight) of one of tea’s major polyphenol antioxidants: epigallocatechin gallate or EGCG.
EGCG is believed responsible for much of green tea’s promise in the prevention of cardiovascular disease, obesity, Alzheimer’s, cancer, periodontal disease and dental cavities.
In addition, EGCG is “gluco-static”. This simply means that EGCG helps prevent sharp rises in blood sugar and consequent spikes in insulin levels: key goals in the prevention and amelioration of diabetes.
The Swiss DSM team, led by Swen Wolfram, PhD, gave severely diabetic mice one of three different doses of EGCG or a placebo, for seven weeks. They then administered glucose-tolerance tests after five weeks and insulin-tolerance tests after six weeks.
The Swiss scientists found that the animals’ glucose tolerance improved after five weeks in a dose-dependent manner, with the effect being most noticeable in mice placed on a very-low-calorie diet.
The EGCG supplement produced reductions in glucose levels of 23, 35, and 48 per cent, with the bigger drops corresponding to the higher doses of the tea extract.
Likewise, the animals’ blood triglyceride levels dropped and their blood insulin levels increased as the doses of EGCG increased.
Dr. Wolfram’s team also reported that EGCG suppressed, beneficially, expression of genes involved in the internal generation of glucose and the synthesis of fatty acids, triglycerides, and cholesterol.
As the DSM group wrote, “To our knowledge, we provide the first evidence that EGCG… exerts potent anti-diabetic activity in vivo in a dose-dependent manner… [and] could potentially improve glucose tolerance in humans with type-2 diabetes mellitus.”
Despite use of an EGCG-rich extract in the successful study, rather than the beverage itself, it seems reasonable to suppose that green tea offers real anti-diabetes potential.
Of course, this expectation assumes that people drink green tea or take a green tea extract frequently.
We will report the results of the planned human trial if and when they become available.
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Green tea sources
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