1. Get the Diabetes Forum App for your phone - available on iOS and Android.
    Dismiss Notice
  2. Guest, we'd love to know what you think about the forum! Take the Diabetes Forum Survey 2021 »
    Dismiss Notice
  3. Diabetes Forum should not be used in an emergency and does not replace your healthcare professional relationship. Posts can be seen by the public.
    Dismiss Notice
  4. Guest, stay home, stay safe, save the NHS. Stay up to date with information about keeping yourself and people around you safe here and GOV.UK: Coronavirus (COVID-19). Think you have symptoms? NHS 111 service is available here.
    Dismiss Notice
Dismiss Notice
Find support, ask questions and share your experiences. Join the community »
Color
Background color
Background image
Border Color
Font Type
Font Size
  1. https://www.lundbeckfonden.com/en/hope-that-a-brain-injection-could-cure-type-2-diabetes/

  2. https://openheart.bmj.com/content/7/2/e001356

  3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6470576/

  4. https://bmcmedicine.biomedcentral.com/articles/10.1186/s12916-020-01688-6

    Insulin shares a limited physiological concentration range with other endocrine hormones. Not only too low, but also too high systemic insulin levels are detrimental for body functions.
  5. https://www.frontiersin.org/articles/10.3389/fendo.2018.00532/full

    This review is motivated by the need to question dogma that has not yielded significant improvements in outcomes of Type 2 Diabetes treatment: that insulin resistance is the driver of ß-Cell failure and resulting hyperglycemia. We highlight the fact that hyperlipidemia, insulin resistance, and hyperinsulinemia all precede overt diabetes diagnosis and can each induce the other when tested experimentally. New research highlights the importance of high levels of circulating insulin as both a driver of weight gain and insulin resistance. Data from our lab and others document that several nutrients and environmental toxins can stimulate insulin secretion at non-stimulatory glucose in the absence of insulin resistance. This occurs either by direct action on the ß-Cell or by shifting its sensitivity to known secretagogues. We raise the next logical question of whether ß-Cell dysfunction in Type 2 Diabetes is due to impaired function, defined as failure, or if chronic overstimulation of the ß-Cell that exceeds its capacity to synthesize and secrete insulin, defined as abuse, is the main abnormality in Type 2 Diabetes. These questions are important as they have direct implications for how to best prevent and treat Type 2 Diabetes.
  6. Here is my 14 days Freestyle experience on IPFS

    https://ipfs.io/ipfs/QmYFvm2rgmziJGysKxDjzr6FoZ16NAD8NkBnJgWp6T9m3Z?filename=Freestyle Libre.pdf
  7. From UW FGF1 research team...
    1. Michael W. Schwartz
    https://diabetes.diabetesjournals.org/content/66/7/1758.long

    Introduction
    Although the brain is clearly capable of affecting blood glucose levels, whether such effects are important in day-to-day blood glucose control remains a matter of controversy. In this Perspective, we update and expand on a previously described brain-centric model of glucose homeostasis (1), highlighting recent evidence of the brain’s capacity to influence the biologically defended level of circulating glucose in part through rapid and highly coordinated adjustments of both insulin sensitivity and insulin secretion. We also discuss the possibility that dysfunction of this brain-centric system contributes to the pathogenesis of type 2 diabetes by raising the defended level of glycemia. Finally, we discuss the implications of these concepts for the future of diabetes treatment.

    Traditionally, the interaction between pancreatic islets and insulin-sensitive tissues has been deemed sufficient to explain most aspects of glucose homeostasis. Whether the brain participates in the physiological control of circulating glucose levels therefore remains a matter of controversy, and the possibility that a dysfunctional central control system contributes to the pathogenesis of diabetes is only beginning to be explored. The overarching goal of this Perspective is to synthesize work from our laboratory and elsewhere that highlights recent progress and identifies emerging research and therapeutic opportunities in these areas.
  8. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3219306/
    upload_2019-8-8_14-30-0.png



    upload_2019-8-8_14-27-12.png
    Neuroprotective effects of ketones
    Neuroprotection is the mechanisms and strategies that, once implemented, may lead to salvage, recovery or regeneration of the nervous system. Ketones may have a neuroprotective effect (see Figure Figure1).1). Ketones represent an alternative fuel for both the normal and the injured brain [43].


    upload_2019-8-8_14-29-8.png

    upload_2019-8-8_14-31-19.png
  9. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4319489/

    Abstract
    There is now an impressive body of literature implicating insulin and insulin signaling in successful aging and longevity. New information from in vivo and in vitro studies concerning insulin and insulin receptors has extended our understanding of the physiological role of insulin in the brain. However, the relevance of these to aging and longevity remains to be elucidated. Here, we review advances in our understanding of the physiological role of insulin in the brain, how insulin gets into the brain, and its relevance to aging and longevity. Furthermore, we examine possible future therapeutic applications and implications of insulin in the context of available models of delayed and accelerated aging.

    upload_2018-5-28_10-31-15.png
  10. https://www.medscape.org/viewarticle/551055

    [​IMG]
  11. The Effect of Medium Chain Triglycerides on Time to Nutritional Ketosis and Symptoms of Keto-Induction in Healthy Adults: A Randomised Controlled Clinical Trial
    https://www.hindawi.com/journals/jnme/2018/2630565/

    Abstract
    Medium chain triglycerides (MCTs) are ketogenic and might reduce adverse effects of keto-induction and improve time to ketosis and the tolerability of very low carbohydrate diets. This study investigates whether MCT supplementation improves time to nutritional ketosis (NK), mood, and symptoms of keto-induction. We compared changes in beta-hydroxybutyrate (BOHB), blood glucose, symptoms of keto-induction, and mood disturbance, in 28 healthy adults prescribed a ketogenic diet, randomised to receive either 30 ml of MCT, or sunflower oil as a control, three times per day, for 20 days. The primary outcome measured was the achievement of NK (≥0.5 mmol·L−1 BOHB). Participants also completed a daily Profile of Mood States and keto-induction symptom questionnaire. MCT resulted in higher BOHB at all time points and faster time to NK, a result that failed to reach significance. Symptoms of keto-induction resulted from both diets, with a greater magnitude in the control group, except for abdominal pain, which occurred with greater frequency and severity in the MCT-supplemented diet. There was a possibly beneficial effect on symptoms by MCT, but the effect on mood was unclear. Based on these results, MCTs increase BOHB compared with LCT and reduce symptoms of keto-induction. It is unclear whether MCTs significantly improve mood or time to NK. The trial was registered by the Australia New Zealand Clinical Trial Registry ACTRN12616001099415.
  12. Attached Files:

  13. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5219747/

    Abstract
    Obesity is a causal factor of type 2 diabetes (T2D); however, people without obesity (including lean, normal weight, or overweight) may still develop T2D. Non-obese T2D is prevalent in Asia and also frequently occurs in Europe. Recently, multiple evidences oppose the notion that either obesity or central obesity (visceral fat accumulation) promotes non-obese T2D. Several factors such as inflammation and environmental factors contribute to non-obese T2D. According to the data derived from gene knockout mice and T2D clinical samples in Asia and Europe, the pathogenesis of non-obese T2D has been unveiled recently. MAP4K4 downregulation in T cells results in enhancement of the IL-6+ Th17 cell population, leading to insulin resistance and T2D in both human and mice. Moreover, MAP4K4 single nucleotide polymorphisms and epigenetic changes are associated with T2D patients. Interactions between MAP4K4 gene variants and environmental factors may contribute to MAP4K4 attenuation in T cells, leading to non-obese T2D. Future investigations of the pathogenesis of non-obese T2D shall lead to development of precision medicine for non-obese T2D.
  • Meet the Community

    Find support, connect with others, ask questions and share your experiences with people with diabetes, their carers and family.

    Did you know: 7 out of 10 people improve their understanding of diabetes within 6 months of being a Diabetes Forum member. Get the Diabetes Forum App and stay connected on iOS and Android

    Grab the app!
  • Tweet with us

  • Like us on Facebook