Special Binding protein extends life of IGF-1, Leads to Incredible Results
Science is finally catching up with what underground bodybuilders have known for years, but may not have known they knew it. IGF-1 is created in the liver when Growth Hormone is present. IGF-1 is responsible for many of the beneficial effects of Growth Hormone, and in some instances counteracts some of the negatives (High does of Growth Hormone cause insulin insensitivity because it makes cells completely reliant on their own triglycerides for energy). There has never been much debate about whether IGF-1 was beneficial to someone with a wasting disease or obesity. The trouble was, injected IGF never seemed to last long enough to gain any benefit from it. What Researchers have discovered however may surprise you.
People with wasting diseases often come up in discussion about fat people. The obese share a common bond with people suffering from HIV, namely their metabolisms have gone out of whack because of excess inflammation from an overactive immune system. People with HIV have a tougher road ahead of them because even all their efforts to control the disease are usually measures intended to simply slow the progression. People who are overweight can terminate their own illness. But that is where the major differences lie really. Both diseases have an almost unbeatable co-morbidity rate (meaning chances are, you will surely die from the disease if you’re not cured).
But this topic isn’t about either one of those groups of people really, even though the study below would lead you to believe that. In fact what we’re talking about here is IGF-1 and a special binding protein called IGFBP-3, Insulin Like Growth Factor Binding Protein Number 3. When bound to IGFBP-3, IGF-1 remains active in the body long enough to enhance weight loss, increase lean muscle mass and reduce almost all markers of prediabetes such as endogenous glucose production and triglycerides. 13 men with HIV who had abdominal adiposity (abnormally fat bellies) and insulin resistance were given 3 months treatment with IGF-1 specially bound to IGFBP-3. The results were nothing short of amazing.
But what I like about this study is it helps shed some light on the whole LR3-IGF-1 use amongst bodybuilders. Their claim is that IGF-1 is rendered useless without a long chain attached to it (that’s the LR3) because it would be quickly bound by proteins and made ineffective. But what this study demonstrates is that the BP3 is actually necessary to help bring about some of the positive effects of IGF-1. Now, there may be people who say that once it’s bound, IGF-1 can no longer work its magic on actual cell hyperplasia (the growth of new muscle cells) and simply becomes nothing more than a fancy glucose disposal agent. To those people I say, you may in fact be right, but for bodybuilders who are on the cusp of insulin resistance and all the metabolic devastation that comes with, something like the worlds most perfect glucose disposal agent could be exactly what they need to thwart metabolic disease while slamming tons of carbs needed for growth and energy.
All in all it looks like we have a promising treatment on the rise from a specially bound form of IGF-1 that could help people who are dying from two very distinct but similar diseases.
J Clin Endocrinol Metab. 2010 Jul 7. [Epub ahead of print]
Effects of Insulin-Like Growth Factor (IGF)-I/IGF-Binding Protein-3 Treatment on Glucose Metabolism and Fat Distribution in Human Immunodeficiency Virus-Infected Patients with Abdominal Obesity and Insulin Resistance.
Rao MN, Mulligan K, Tai V, Wen MJ, Dyachenko A, Weinberg M, Li X, Lang T, Grunfeld C, Schwarz JM, Schambelan M.
Department of Medicine (M.N.R., K.M., M.J.W., M.W., C.G., J.-M.S., M.S.) and Center for Molecular and Functional Imaging (X.L., T.L.), University of California, San Francisco, San Francisco, California 94143; Division of Endocrinology (M.N.R., K.M., V.T., M.W., J.-M.S., M.S.), San Francisco General Hospital, San Francisco, California 94110; Touro University (A.D., J.-M.S.), Vallejo, California 94592; and Division of Metabolism and Endocrinology (C.G.), Veterans Affairs Medical Center, San Francisco, California 94121.
Abstract
Context: HIV-infected patients on antiretroviral therapy are at increased risk for excess visceral adiposity and insulin resistance. Treatment with GH decreases visceral adiposity but worsens glucose metabolism. IGF-I, which mediates many of the effects of GH, improves insulin sensitivity in HIV-negative individuals. Objective: Our objective was to determine whether IGF-I, complexed to its major binding protein, IGF-binding protein-3 (IGFBP-3), improves glucose metabolism and alters body fat distribution in HIV-infected patients with abdominal obesity and insulin resistance. Methods: We conducted a pilot, open-label study in 13 HIV-infected men with excess abdominal adiposity and insulin resistance to assess the effect of 3 months of treatment with IGF-I/IGFBP-3 on glucose metabolism and fat distribution. Glucose metabolism was assessed by oral glucose tolerance test and hyperinsulinemic-euglycemic clamp. Endogenous glucose production (EGP), gluconeogenesis, whole-body lipolysis, and de novo lipogenesis (DNL) were measured with stable isotope infusions. Body composition was assessed by dual-energy x-ray absorptiometry and abdominal computed tomography scan. Results: Glucose tolerance improved and insulin-mediated glucose uptake increased significantly during treatment. EGP increased under fasting conditions, and suppression of EGP by insulin was blunted. Fasting triglycerides decreased significantly in association with a decrease in hepatic DNL. Lean body mass increased and total body fat decreased, whereas visceral adipose tissue did not change. Conclusions: Treatment with IGF-I/IGFBP-3 improved whole-body glucose uptake and glucose tolerance, while increasing hepatic glucose production. Fasting triglycerides improved, reflecting decreased DNL, and visceral adiposity was unchanged.
PMID: 20610601 [PubMed - as supplied by publisher]
