is anyone taking this drug for their diabetes?

Swedes Show Byetta Cures Parkinson's Disease in Rats

7-Sep-07
Peptide hormone exendin-4 stimulates subventricular zone neurogenesis in the adult rodent brain and induces recovery in an animal model of parkinson's disease.

Bertilsson G, Patrone C, Zachrisson O, Andersson A, Dannaeus K, Heidrich J, Kortesmaa J, Mercer A, Nielsen E, R?olm H, Wikstr?.

NeuroNova AB, Stockholm, Sweden.

We investigated the effects of exendin-4 on neural stem/progenitor cells in the subventricular zone of the adult rodent brain and its functional effects in an animal model of Parkinson's disease. Our results showed expression of GLP-1 receptor mRNA or protein in the subventricular zone and cultured neural stem/progenitor cells isolated from this region.

In vitro, exendin-4 increased the number of neural stem/progenitor cells, and the number of cells expressing the neuronal markers microtubule-associated protein 2, beta-III-tubulin, and neuron-specific enolase.

When exendin-4 was given intraperitoneally to naive rodents together with bromodeoxyuridine, a marker for DNA synthesis, both the number of bromodeoxyuridine-positive cells and the number of neuronal precursor cells expressing doublecortin were increased.

Exendin-4 was tested in the 6-hydroxydopamine model of Parkinson's disease to investigate its possible functional effects in an animal model with neuronal loss. After unilateral lesion and a 5-week stabilization period, the rats were treated for 3 weeks with exendin-4. We found a reduction of amphetamine-induced rotations in animals receiving exendin-4 that persisted for several weeks after drug administration had been terminated.

Histological analysis showed that exendin-4 significantly increased the number of both tyrosine hydroxylase- and vesicular monoamine transporter 2-positive neurons in the substantia nigra.

In conclusion, our results show that exendin-4 is able to promote adult neurogenesis in vitro and in vivo, normalize dopamine imbalance, and increase the number of cells positive for markers of dopaminergic neurons in the substantia nigra in a model of Parkinson's disease.

I have no idea what this article actually says because I have a black hole where everything scientific just gets sucked in -never to be heard from again. HOWEVER....there is no doubt in my mind, that at least in my case, there is an unquestionable connection between my PD and how my body handles Glucose (actually, food in general). How long has this drug been on the Market? I am not technically a diabetic, but I sure have grief with hyper/hypo glycemia. I suspect the root of the problem is insulin resistance.
Carolyn is our resident diabetic, she would be the one to ask.

byetta received approval april, 2005, so is a relatively new drug on the market. It mimics a glucagon hormone in its action for diabetes. It also acts like a neurotropic factor (like GDNF, BDNF)in experiments with both cultured cells and adult mice --in mice, new neuron growth appeared, the # of dopamine producing cells increased in the substantia nigra, and dopamine balance was "normalized" ("increased the number of both tyrosine hydroxylase- and vesicular monoamine transporter 2-positive neurons in the substantia nigra").

In plain english what does this mean? Do we have to worry that if we do not have a problem with blood sugar levels that this drug will cause such,etc.....I used to work as a medic pre PD and once had a guy who was unconscious after taking what he thought was a cheap score on some valium.
Turns out it was diabeta-lowered his blood sugar so bad that he almost checked out.

You can read more about Byetta here:

http://www.byetta.com/index.jsp

It is not popular however, not making it well in the common sector or in nursing homes.

I think this is connected to type III diabetes...that is the BRAIN makes insulin and there must be a connection to PD when this fails.

You know there were posts on inositol...at one time on this forum or at OBT, I can't recall which...because inositol improves glucose utilization in the brain.
I wonder if that is related here? There are mixed opinions on this however..but insulin resistance does respond to inositol use. (diabetics lose this nutrient normally in the urine for some reason-- so need supplements of it).

http://www.byetta.com/hcp/glp-1_effe...p?reqNavId=1.4

this drug is Glucagon-like peptide-1 (GLP-1) an important incretin hormone secreted by L-cells in the small intestine and colon in response to food intake. As its name might imply, GLP-1 is structurally similar to glucagon. However, they are entirely different hormones and the function of GLP-1 is significantly different from that of glucagon.

GLP-1 acts by binding to specific receptors on the surface of the beta cell, as well as other tissues, and has a very short half-life (less than 2 minutes in the circulation). GLP-1 exerts multiple effects that contribute to the maintenance of glucose homeostasis:

Enhances glucose-dependent insulin secretion1,2
Suppresses inappropriate glucagon secretion1,2
Promotes satiety, leading to reduction of food intake1
Regulates the rate of gastric emptying, limiting postprandial glucose excursions1,2


GLP-1 enhances insulin secretion only in the presence of elevated glucose concentrations.


Insulin secretion
GLP-1 stimulates insulin secretion from beta cells in the pancreas in a glucose-dependent manner:

Stimulates secretion of insulin only when the glucose concentration is elevated
When glucose concentration returns toward normal, this effect of GLP-1 declines
The glucose-dependent nature of GLP-1 prevents too much insulin from being secreted, thus decreasing the risk of hypoglycemia.


Postprandial GLP-1 levels are reduced in patients with
type 2 diabetes.


Glucagon secretion
Glucagon is a hormone that causes the release of glucose from the liver in order to maintain normal glucose homeostasis during fasting and is an important protective mechanism against hypoglycemia. Conversely, glucagon secretion is suppressed during periods of hyperglycemia.

GLP-1 suppresses glucagon secretion from alpha cells in the pancreas in a glucose-dependent manner:

Suppresses glucagon secretion in the fed state
During hypoglycemia, glucagon suppression does not occur
In patients with type 2 diabetes, glucagon concentrations are often inappropriately elevated, resulting in increased hepatic glucose output and postprandial glucose excursions.

Satiety
The central nervous system is a critical site for regulating food intake, satiety, and body weight. GLP-1 works on the brain to trigger a feeling of satiety and reduce food intake.

Gastric emptying
The rate of gastric emptying is a key determinant of the rate of nutrient absorption, an important factor in postprandial glucose excursions. GLP-1 slows the rate of gastric emptying, which in turn slows the delivery and absorption of nutrients in the small intestine and thereby limits the rate at which carbohydrate is absorbed into the circulation. The rate of gastric emptying is often increased in patients with type 2 diabetes, causing a rapid rise in postprandial blood glucose.

1 Zander M, Madsbad S, Madsen JL, et al. Effect of 6-week course of glucagon-like peptide 1 on glycaemic control, insulin sensitivity, and beta-cell function in type 2 diabetes: a parallel-group study. Lancet. 2002;359:824-830.
2 Nauck MA, Wollschlager D, Werner J, et al. Effects of subcutaneous glucagon-like peptide 1 (GLP-1 [7-36 amide]) in patients with NIDDM. Diabetologia. 1996;39:1546-1553.