Type 2 Diabetes:

Relevance to autoimmune diabetes management and prevention.

Insulitis in autoimmune diabetes involves the infiltration of activated macrophages and dendritic cells to the pancreatic , and islet 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 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 IDDMonset 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 neighbouring 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.


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.


1. 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.
2. 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.
3. 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
4. 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.
5. Porte D Jr. Banting Lecture 1991: beta-cells in type 2 diabetes mellitus. Diabetes 1991. 40:166-180.
6. ScienceDaily. Retrieved November 30, 2007, from