Please Scroll Down to See Forums Below 
Is this saying what I think it is? I've been doing some research on ALA and while I have no back ground on anything regarding these test, I found that this may be talking about ALA keeping fat storages from enlarging. I could be wrong and if this study has already be posted somewhere on this board I apologize!
------------------------
Author(s): Greene EL; Nelson BA; Robinson KA; Buse MG
Author's Address: Division of Endocrinology, Department of Internal Medicine, Medical University of South Carolina, Charleston, SC 29425, USA.
Title: alpha-Lipoic acid prevents the development of glucose-induced insulin resistance in 3T3-L1 adipocytes and accelerates the decline in immunoreactive insulin during cell incubation.
Language: English
Source: Metabolism, 2001 Sep; Vol. 50 (9), pp. 1063-9.
Country: United States
ISSN: 0026-0495
Pub. Type: Journal Article
Journal ID(s): Journal Code: MUM NLM ID: 0375267
Subset: IM
MeSH Heading: Adipocytes:CY/DE/*ME. Glucose:*ME/PD. Insulin:*ME/PD. Insulin Resistance:*PH. Thioctic Acid:*AA/*PD. 3T3 Cells. Acetylcysteine
D. AntioxidantsD. Biological Transport
E. Culture Media, Conditioned:CH/ME. Dose-Response Relationship, Drug. Drug Synergism. Mice. Oxidative StressE. Animal. Support, Non-U.S. Gov't. Support, U.S. Gov't, P.H.S.
Abstract: Oxidative stress has been implicated in glucose toxicity. We tested the hypothesis that certain antioxidants may prevent insulin-resistant glucose transport that develops in adipocytes after sustained exposure to high glucose, provided insulin is present. The antioxidant alpha-lipoic acid has been proposed as an insulin sensitizer. 3T3-L1 adipocytes were preincubated 18 hours in media containing insulin (0.6 nmol/L) with low (5 mmol/L) or high (25 mmol/L) glucose with or without alpha-lipoate, dihydrolipoate (each 0.1 to 0.5 mmol/L), or N-acetylcysteine (1 to 5 mmol/L). After extensive re-equilibration in insulin and antioxidant-free media, basal and maximally insulin-stimulated (100 nmol/L) glucose transport was measured. Insulin was quantified by radioimmunoassay. Preincubation with alpha-lipoate and dihydrolipoate but not N-acetylcysteine increased subsequent basal glucose transport; the effect was much smaller than that of acute maximal insulin stimulation. Preincubation in high glucose without antioxidants inhibited acutely insulin-stimulated glucose transport by 40% to 50% compared with low glucose. This down- regulation was partially or completely prevented by each antioxidant. In cell-free media, the 2 reductants, dihydrolipoate and N-acetylcysteine, rapidly decreased immunoreactive insulin, but alpha-lipoate was ineffective. However, during incubation with adipocytes, alpha-lipoate, and dihydrolipoate promoted the decline in immunoreactive insulin nearly equally. Because insulin and high glucose are synergistic in inducing insulin resistance in this model, the reduction in immunoreactive insulin probably contributed to the protective effect of the antioxidants. 3T3-L1 adipocytes efficiently metabolize alpha-lipoate to dihydrolipoate, which may be released into the medium. The stimulation of glucose transport by alpha-lipoic acid may represent redox effects in subcellular compartments that are accessible to dihydrolipoate. (Copyright 2001 by W.B. Saunders Company)
Grant Information: GM-08716-01 GM NIGMS; K01 HL-03710 HL NHLBI; R01 DK-02001 DK NIDDK
CAS Registry #: 0 (Antioxidants)
0 (Culture Media, Conditioned)
11061-68-0 (Insulin)
462-20-4 (dihydrolipoic acid)
50-99-7 (Glucose)
616-91-1 (Acetylcysteine)
62-46-4 (Thioctic Acid)
Entry Date(s): Date Created: 20010913 Date Completed: 20011018
Citation ID(s): Medline UI: 21439666 PMID: 11555840
------------------------
Author(s): Greene EL; Nelson BA; Robinson KA; Buse MG
Author's Address: Division of Endocrinology, Department of Internal Medicine, Medical University of South Carolina, Charleston, SC 29425, USA.
Title: alpha-Lipoic acid prevents the development of glucose-induced insulin resistance in 3T3-L1 adipocytes and accelerates the decline in immunoreactive insulin during cell incubation.
Language: English
Source: Metabolism, 2001 Sep; Vol. 50 (9), pp. 1063-9.
Country: United States
ISSN: 0026-0495
Pub. Type: Journal Article
Journal ID(s): Journal Code: MUM NLM ID: 0375267
Subset: IM
MeSH Heading: Adipocytes:CY/DE/*ME. Glucose:*ME/PD. Insulin:*ME/PD. Insulin Resistance:*PH. Thioctic Acid:*AA/*PD. 3T3 Cells. Acetylcysteine
D. AntioxidantsD. Biological TransportE. Culture Media, Conditioned:CH/ME. Dose-Response Relationship, Drug. Drug Synergism. Mice. Oxidative StressE. Animal. Support, Non-U.S. Gov't. Support, U.S. Gov't, P.H.S. Abstract: Oxidative stress has been implicated in glucose toxicity. We tested the hypothesis that certain antioxidants may prevent insulin-resistant glucose transport that develops in adipocytes after sustained exposure to high glucose, provided insulin is present. The antioxidant alpha-lipoic acid has been proposed as an insulin sensitizer. 3T3-L1 adipocytes were preincubated 18 hours in media containing insulin (0.6 nmol/L) with low (5 mmol/L) or high (25 mmol/L) glucose with or without alpha-lipoate, dihydrolipoate (each 0.1 to 0.5 mmol/L), or N-acetylcysteine (1 to 5 mmol/L). After extensive re-equilibration in insulin and antioxidant-free media, basal and maximally insulin-stimulated (100 nmol/L) glucose transport was measured. Insulin was quantified by radioimmunoassay. Preincubation with alpha-lipoate and dihydrolipoate but not N-acetylcysteine increased subsequent basal glucose transport; the effect was much smaller than that of acute maximal insulin stimulation. Preincubation in high glucose without antioxidants inhibited acutely insulin-stimulated glucose transport by 40% to 50% compared with low glucose. This down- regulation was partially or completely prevented by each antioxidant. In cell-free media, the 2 reductants, dihydrolipoate and N-acetylcysteine, rapidly decreased immunoreactive insulin, but alpha-lipoate was ineffective. However, during incubation with adipocytes, alpha-lipoate, and dihydrolipoate promoted the decline in immunoreactive insulin nearly equally. Because insulin and high glucose are synergistic in inducing insulin resistance in this model, the reduction in immunoreactive insulin probably contributed to the protective effect of the antioxidants. 3T3-L1 adipocytes efficiently metabolize alpha-lipoate to dihydrolipoate, which may be released into the medium. The stimulation of glucose transport by alpha-lipoic acid may represent redox effects in subcellular compartments that are accessible to dihydrolipoate. (Copyright 2001 by W.B. Saunders Company)
Grant Information: GM-08716-01 GM NIGMS; K01 HL-03710 HL NHLBI; R01 DK-02001 DK NIDDK
CAS Registry #: 0 (Antioxidants)
0 (Culture Media, Conditioned)
11061-68-0 (Insulin)
462-20-4 (dihydrolipoic acid)
50-99-7 (Glucose)
616-91-1 (Acetylcysteine)
62-46-4 (Thioctic Acid)
Entry Date(s): Date Created: 20010913 Date Completed: 20011018
Citation ID(s): Medline UI: 21439666 PMID: 11555840
