Diabetes
Blood sugar levels are regulated in a negative feedback loop, which consists of the hormones insulin and glucagon.
The following illustration clearly depicts this.
When blood sugar levels get too low the regulatory hormone glucagon is produced which is then able to bring these levels back into a normal range. Alpha cells, which are specialized cells found in the pancreas, produce glucagon. In turn, when blood sugar levels become too high, beta cells, also found in the pancreas, produce insulin. It is the responsibility of Insulin to facilitate the movement of glucose into cells and out of the blood. In this manner blood sugar levels are brought back into normal range. When glucose does not adequately enter cells, blood glucose levels remain high and Diabetes, also referred to as hyperglycemia, is the result.
The condition of diabetes is consists of two main categories. The types and characteristics of each are as follows:
*Type I- Onset of type I diabetes generally occurs early in life which is why it is often referred to as "juvenile onset" diabetes. It is also known as IDDM (insulin dependent diabetes mellitus) because it usually requires medication or insulin injections. There are two areas of speculation as to the cause of this type of diabetes. First, some believe that an autoimmune response occurs toward the beta cells causing the body to destroy them, which results in a reduced level of insulin. Second, others speculate that a serious infection is the cause of the destruction of beta cells, resulting in reduced insulin.
*Type II- The onset of type II diabetes generally occurs later in life which is why it is termed as "adult onset" diabetes. Another name for type II diabetes is NIDDM (non-insulin dependent diabetes mellitus). Many people with this type of diabetes can regulate their blood glucose levels with a proper diet and exercise. In type II diabetes glucose levels are elevated, not because the body isn't producing enough insulin, but because the cells do not respond to the insulin being produced. When cells do not respond to insulin, glucose cannot be transferred into them. This kind of diabetes is much more common than type I. Obesity, lack of exercise, and aging all play a role in the development of type II diabetes.
Research conducted in the area of diabetes with nutritional or herbal support is as follows:
*Essential fatty acids- In Med Hypotheses May 2000; 54(5): 786-93 essential fatty acids like CLA (conjugated linoleic acids) may aid in glycemic (blood glucose) control which could help prevent type II diabetes.
*Antioxidants-In Diabetes Metabolism May 2000; 26(3): 63-76 high glucose concentrations are said to cause oxidative stress, or an imbalance of free radicals and antioxidants. Antioxidant supplementation is discussed in diabetic conditions.
*Transfer factors-Because of the immune system's involvement in type I diabetes immunotherapy has been researched. In an induced diabetic condition the inducer and suppressor components of transfer factor molecules showed an anti-diabetic effect. More information about this can be found in Biotherapy 1996; 9: 149-157.
*Gymnema sylvestre- J Ethnopharmacol 1990 Oct; 30(3): 265-79 discusses the ability of this extract to possibly bring about normal blood glucose levels by a regeneration of beta cells in type I diabetes. A common name for gymnema sylvestre is gurmar.
Because there is a lot of variation among diabetic conditions these supplements may not be appropriate for everyone.
Research and Development
Dialyzable lymphoid extract (DLE) from mice resistant to STZ-induced diabetogenesis can interrupt the progress of diabetes in STZ-treated CD-1 mice.
Borkowsky W, Pilson R, Lawrence HS.
New York University Medical Center. Department of Paediatrics, New York, NY, USA.
DLE was prepared from the minority of euglycemic CD-1 mice, previously injected with STZ, and was administered to hyperglycemic CD-1 male mice 1, 2 and 3 weeks after completion of multidose STZ. Mice treated with DLE derived from 2 x 10(7) (IX) or 10(8) lymphocyte equivalents (lymph.equ) were significantly less hyperglycemic than the saline treated controls (P < 0.001). The effects of DLE remained evident for more than 10 weeks after the final DLE treatment. Mice treated with DLE prepared from diabetic mice (hg DLE) developed a somewhat more rapid onset of hyperglycemia than the STZ treated control animals, although this effect did not achieve statistical significance (P = 0.1). This DLE was absorbed on a rat insulinoma cell line (RIN), which contains interspecies cross-reacting islet antigens, and compared to the unabsorbed DLE. Mice treated with hg DLE preabsorbed on RIN cells, showed a slower onset of hyperglycemia. DLE prepared from euglycemia mice and the RIN-absorbed fraction were equally capable of preventing hyperglycemia (P < 0.05). In order to determine whether the DLE effects were genetically restricted, DLE was prepared from BALB/c mice, normally resistant to the diabetogenic effects of multidose STZ, both before and after STZ treatment. STZ primed CD-1 mice treated with 3 weekly doses of 2 x 10(7) lymph. equ. of untreated BALB/c derived DLE, STZ treated BALB/c derived DLE, and STZ treated CD-1 DLE were all less hyperglycemic than the control mice, who received saline (P < 0.001). However, mice treated with CD-1 DLE were less hyperglycemic than the mice given BALB/c derived DLE (P < 0.05). These effects were relatively long-lived. Mice that were given the > 3,500 Dalton fraction of CD-1 DLE were significantly less hyperglycemic than either the control mice or those treated with the < 3,500 Dalton fraction of CD-1 DLE (P < 0.05). Effects remained evident for more than 3 months after the last dose of DLE. Pancreatic tissue from the mice treated with the > 3,500 Dalton fraction of CD-1 derived DLE revealed slightly more islets of a slightly greater size with less surrounding inflammation than either control mice or mice treated with the < 3,500 Dalton fraction of DLE.
PMID: 8993774 [PubMed - indexed for MEDLINE