Diabetogenic Impact Of Long-chain Omega-3 Fatty Acids On Pancreatic Beta-cell Function And The Regul

Discussion in 'Articles & Scientific Studies' started by paymanz, Feb 20, 2017.

  1. paymanz

    paymanz Member

    Joined:
    Jan 6, 2015
    Messages:
    2,630
    Gender:
    Male
    Diabetogenic impact of long-chain omega-3 fatty acids on pancreatic beta-cell function and the regulation of endogenous glucose production. - PubMed - NCBI


    Abstract

    In healthy individuals, peripheral insulin resistance evoked by dietary saturated lipid can be accompanied by increased insulin secretion such that glucose tolerance is maintained. Substitution of long-chain omega-3 fatty acids for a small percentage of dietary saturated fat prevents insulin resistance in response to high-saturated fat feeding. We substituted a small amount (7%) of dietary lipid with long-chain omega-3 fatty acids during 4 wk of high-saturated fat feeding to investigate the relationship between amelioration of insulin resistance and glucose-stimulated insulin secretion (GSIS). We demonstrate that, despite dietary delivery of saturated fat throughout, this manipulation prevents high-saturated fat feeding-induced insulin resistance with respect to peripheral glucose disposal and reverses insulin hypersecretion in response to glucose in vivo. Effects of long-chain omega-3 fatty acid enrichment to lower GSIS were also observed in perifused islets suggesting a direct effect on islet function. However, long-chain omega-3 fatty acid enrichment led to hepatic insulin resistance with respect to suppression of glucose output and impaired glucose tolerance in vivo. Our data demonstrate that the insulin response to glucose is suppressed to a greater extent than whole-body insulin sensitivity is enhanced by enrichment of a high-saturated fat diet with long-chain omega-3 fatty acids. Additionally, reduced GSIS despite glucose intolerance suggests that either long-chain omega-3 fatty acids directly impair the beta-cell response to saturated fat such that insulin secretion cannot be augmented to normalize glucose tolerance or beta-cell compensatory hypersecretion represents a response to insulin resistance at the level of peripheral glucose disposal but not endogenous glucose production
     
  2. pboy

    pboy Member

    Joined:
    Jan 22, 2013
    Messages:
    1,681
    I don't even know what they are saying there to be honest, but it seems like its saying long chains mess with metabolism in liver and pancreas but might aid peripheral glucose usage? so you have people saying long chain omegas might do x and y that are good and others saying x and y that are bad...so I trust senses and say am I compelled to the smell of fish and fiend for it on days I have none as I would food with other nutrients? its never happened...like if I'm low in a b vitamin or mineral, within a day or really soon after if happens ill start getting cravings for things that have it or feel deprived somehow...maybe 'full' but not satisfied totally...that's never happened with pufa's to be honest so I don't think theyre necessary or if so its under a gram or even less
     
  3. OP
    paymanz

    paymanz Member

    Joined:
    Jan 6, 2015
    Messages:
    2,630
    Gender:
    Male
    According to ray omega3s are anti inflammatory,

    And one cause of insuline resistance is inflammation. So it maybe improve insuline sensitivity because of that.(but in long term it probably cause more inflammation and damage because of oxidative stress)

    And In one of his interviews recently he mentioned type one diabetes is caused mainly by peroxides generated from PUFA which destroys beta cells.

    That interview KMUD: 10-21-16 Rheumatoid Arthritis
     
Loading...