Sat, Nov-12-11, 11:49
|
 |
Senior Member
Posts: 15,075
|
|
Plan: mostly milkfat
Stats: 190/152.4/154
BF:
Progress: 104%
Location: Ontario
|
|
Quote:
|
To truly address this question, we need to consider targeted experiments that increase circulating insulin over long periods of time without altering a number of other factors throughout the body.
|
I don't think any of the studies Stephan posted meet this requirement. This one, for instance;
http://diabetes.diabetesjournals.or.../50/5/1110.long
Quote:
|
Liver-Specific igf-1 Gene Deletion Leads to Muscle Insulin Insensitivity
|
Results in not only increased insulin, but also increased growth hormone.
Quote:
|
GH concentrations from single samples in individual mice by RIA indicated that the serum GH levels were markedly increased in the liver-specific KO mice (2.8 ± 0.5 ng/ml in the L/L− mice vs. 17.8 ± 11 ng/ml in the L/L+ mice P = 0.01).
|
This bit about insulin mimetics;
Quote:
|
In an interesting 2002 study, researchers orally administered a small molecule insulin mimetic (drug that mimics insulin action) to mice and placed them on an obesity-promoting diet. Mice that received this treatment gained less fat than mice that were not given the drug over the course of six weeks (7), consistent with insulin's ability to constrain fat mass by acting in the brain (8).
|
http://www.ncbi.nlm.nih.gov/pubmed/11821903
Quote:
|
Obesity and insulin resistance are major risk factors for a number of metabolic disorders, such as type 2 diabetes mellitus. Insulin has been suggested to function as one of the adiposity signals to the brain for modulation of energy balance. Administration of insulin into the brain reduces food intake and body weight, and mice with a genetic deletion of neuronal insulin receptors are hyperphagic and obese. However, insulin is also an anabolic factor; when administered systemically, pharmacological levels of insulin are associated with body weight gain in patients. In this study, we investigated the efficacy and feasibility of small molecule insulin mimetic compounds to regulate key parameters of energy homeostasis. Central intracerebroventricular (i.c.v.) administration of an insulin mimetic resulted in a dose-dependent reduction of food intake and body weight in rats, and altered the expression of hypothalamic genes known to regulate food intake and body weight. Oral administration of a mimetic in a mouse model of high-fat diet-induced obesity reduced body weight gain, adiposity and insulin resistance. Thus, insulin mimetics have a unique advantage over insulin in the control of body weight and hold potential as a novel anti-obesity treatment.
|
Insulin and insulin mimetics to the brain decrease hunger and bodyweight. Leptin also does this. All of these will increase nutrition to a cell on a local basis; they encourage the cell to take in nutrients. So maybe you end up with cells in the hypothalamus clearing more glucose from the blood, and then sending a "sated" signal to the body. Insulin injected into the arm will also increase nutrition locally over time, inject insulin in the same place for years, and fat will accumulate. But this insulin doesn't act just in the brain, it's systemic; and if every cell in the body tries to pull in more glucose at the same time, maybe the animal ends up hungry instead of sated.
An insulin mimetic isn't insulin. Leptin acts as an insulin mimetic, several studies have shown that it can be used, in large amounts, to control blood glucose under type I conditions. Any suggestion that leptin, as an insulin mimetic, needs to be a cause of obesity in order for excess insulin to be a cause of obesity, would be silly. You might expect an insulin mimetic to lower insulin requirements, and maybe by doing this lower insulin secretion and some of the consequences of insulin secretion. |
Linear Mode
