|
The established
immune modulating properties of Qina obtrudes the question
of how can this
be utilized
in the treatment and management of diabetes.
Relevance to
autoimmune diabetes management and prevention
Insulitis in autoimmune
diabetes involves the infiltration of activated macrophages
and dendritic cells to the pancreatic islet, and these are followed by greater numbers of effector CD4+ and CD8+ lymphocytes
1-2. This series of events then leads to the production
of pro-inflammatory cytokines and reactive oxygen radicals
(ROR) of which Nitric Oxide (NO) is one. The cytokines are
capable of mediating two types of effector functions leading
to the destruction of ß-cells. First, they could exert direct
toxicity to these target cells 3. Second, the
cytokines have also been shown to trigger pancreatic beta-cells
to produce
ROR 4. Pancreatic beta-cells have low capability
to scavenge free radicals, and the local accumulation of
ROR would therefore
contribute to their damage. In this context, there is a rationale
for using Qina to modulate the effect of NO in order to prevent
further ß-cell damage. Whether Qina may actually contribute
to a delay in IDDM onset has not yet been tested
Relevance
to type 2 diabetes management
The development of type
2 diabetes is characterized by the malfunction of the pancreatic
beta-cells in combination with insulin resistance.
To overcome insulin resistance, beta-cells tend to increase
their production of insulin. However, in situations where
insufficient
insulin is produced, the onset of glucose intolerance
occurs 5. Researchers at the University of California, San
Diego (UCSD) School of Medicine have discovered that inflammation
provoked by immune cells called macrophages leads to
insulin
resistance and Type 2 diabetes6.
Macrophages, found in
white blood cells in the bone marrow, are key players in
the immune
response. When these immune cells get into tissues,
such as adipose or liver tissue, they release cytokines,
which
are chemical messenger molecules used by immune and
nerve cells
to communicate. These cytokines cause the neighboring
liver, muscle or fat cells to become insulin resistant, which
in turn can lead to Type 2 diabetes.
The UCSD research team showed
that the macrophage is the cause of this cascade
of events by knocking out a key component of the inflammatory
pathway in the macrophage. The research also proved
that obesity without inflammation does not result in insulin
resistance. When an animal or a human being becomes obese, they
develop
steatosis, or increased fat in the liver. The steatosis
leads
to liver inflammation and hepatic insulin resistance.
Conclusion
It is proven that, by disabling the macrophage inflammatory pathway,
insulin resistance and the resultant Type 2 diabetes can
be prevented. . Whilst the exact mechanisms mediated by Qina are
currently
unknown, existing studies at least show that Qina
is indeed efficacious in inhibiting inflammation, abolishing
reactive oxygen species and improving hyperglycemia by modulation
of the macrophage which induces and controls the immune
inflammatory
response. This innovative approach may prove superior
in the regulation of glucose control and improved management
of Type-II diabetes as
an adjuvant to known therapies.
References
- Jansen A, Homo-Delarche F,
Hooijkaas H, Leenen PJ, Dardenne M, Drexhage HA. Immunohistochemical
characterisation of monocytes-macrophages and dendritic
cells involved in the initiation of the insulitis and beta
cell destruction in NOD mice. Diabetes 1994. 43:667-675.
- Kay TW, Chaplin HL, Parker
JL, Stephens LA, Thomas HE. CD4+ and CD8+ T lymphocytes:
clarification of their pathogenic roles in diabetes in
the NOD mouse. Res Immunol 1997. 148:320-327.
- Rabinovitch A, Suarez-Pinzon
WL. Cytokines and their roles in pancreatic islet beta-cell
destruction and insulin-dependent diabetes mellitus. Biochem
Pharmacol 1998. 55:1139-1149
- Lotz S, Tiedge M, Nachtwey
T, Karlsen AE, Nerup J, Lenzen S. Protection of insulin-producing
RINm5F cells against cytokine-mediated cytoxicity through
overexpression of antioxidant enzymes. Diabetes 2000. 49:1123-1130.
- Porte D Jr. Banting Lecture
1991: beta-cells in type 2 diabetes mellitus. Diabetes
1991. 40:166-180.
- ScienceDaily. Retrieved November 30, 2007, from http://www.sciencedaily.com /releases/2007/11/071106133106.htm
|
