Episode 26 - Dr.Bikman: well behaved fat and good insulin signaling FTW

by Break Nutrition | Podcast

Discuss further on: https://ask.breaknutrition.com

Show notes:

    • Here’s Dr.Bikman’s Twitter profile
    • The Bikman lab is in The College of Life Sciences of Brigham Young University
      • It focuses on identifying first “the molecular mechanisms that explain the increased risk of disease that accompanies weight gain, with particular emphasis on the etiology of insulin resistance and disrupted mitochondrial function. Second, we hope to reveal novel cellular processes that are responsible for fat development”
    • Dr.Bikman enumerates some of the metabolic drugs used in disease like diabetes, cancer and Alzheimer’s, pointing to Metformin as a particularly effective one given its ability to improve insulin sensitivity
    • Fat cells (adipocytes) are studied by Dr.Bikman’s lab, specifically regarding their regulation of metabolic rate. This has been a very fun area of research for him.
    • Uncoupling, whereby the mitochondrial electron transport chain generates heat by being uncoupled from ATP production, may be involved in explaining supposed ‘metabolic advantages’ of diets low in dietary carbohydrate
    • Human subcutaneous (under the skin) fat stores most of our energy and it’s primarily white adipose tissue (WAT) but can beige like brown adipose tissue (BAT)
    • Dr.Bikman noticed that, unlike subcutaneous fat, visceral fat struggles to shift from the coupled to uncoupled state
    • I bring up the old wives tale of the cold helping people lose fat. I mention having experimented with cold-exposure (ice baths, cold showers…) and being impressed by my improved thermoregulation
    • Dr.Bikman also takes cold showers and anecdotally reports catching fewer colds and flus
    • Dr.Bikman and colleagues have a recent publication in the Journal of Insulin Resistance called β-Hydroxybutyrate improves β-cell mitochondrial function and survival
      • The study looked at how pancreatic cells, specifically the beta-cells secreting insulin in response to glucose (amongst other things), behave in the presence or absence of the ketone bodies beta-hydroxybutyrate (BhB)
      • Dr.Bikman’s data revealed a interesting observations in need of further study
        • βHB does not enhance insulin production; type 2 diabetics usually chronically secrete too much insulin
        • But βHB increased ATP production whilst elevating the Phosphate-to-Oxygen (PO) ratio; in effect the amount of ATP per unit oxygen increased. Pancreatic beta-cells die off when they can’t maintain adequate pools of ATP
        • Yet, the ATP:insulin ratio was similar between Control cells and βHB-fed cells ⇒ this is hard to explain since ATP increased whilst insulin didn’t increase, so why isn’t the ATP:insulin ratio higher in BhB fed cells?
          • Dr.Bikman speculates that this result is an artifact of this cell culture model being a little to artificial, or a solution of BhB ketones simply doesn’t stimulate the beta-cell’s insulin secretion
      • A little about the study design and methods
        • INS-1 832/13 cancer beta-cells from the pancreas of rats ‘thrive’ in vitro when fed ketones
        • Cells were fed palmitate for 24hrs ⇒ 40% of water-controls survived vs 50% of ketone fed ones
        • “As both assays measure cellular NADPH and NADH levels, these data demonstrate increased viability through either increased proliferation or mitochondrial function
    • Here are some basics of what goes on inside the electron transport chain (ETC) as explained by Petro from Hyperlipid to contextualise Dr.Bikman’s results
      • Glucose favours Complex I, fat favours Complex II
        • “Complex II is actually the succinate dehydrogenase enzyme of the citric acid cycle. It is built into the wall of the inner mitochondrial membrane and hands its electrons to the CoQ pool directly, no Complex I involved. Another difference is that Complex II doesn’t pump any protons
    • Excellent point in the Discussion section ⇒ “interventions aimed at restoring inherent β-cell function should be encouraged to help avoid exogenous insulin therapy and its consequences
    • whereas primary islets tended towards enhanced insulin section, INS-1 832/13 β-cells tended towards reduced insulin secretion
      • I raise the possibility that, according to this difference between INS-1 and primary islet cells, BhB could contribute to normal insulin secretion in healthy (primary islet) cells whilst reducing insulin secretion in cancerous ones ⇒ this could resembles features of safe metabolic cancer therapies
    • Excellent point in the Conclusion section ⇒ “Perhaps in response to and in parallel with the immune-mediated loss of pancreatic β-cells, hepatic ketogenesis is a mechanism that, in addition to other ends, attempts to maintain and even restore β-cell survival
      • It suggests ketone molecules or ketone generating interventions could have a role in the treatment of diabetes (and possibly diseases of insulin resistance)
  • Younger bioenergetics student Ben Bikman realized the simplistic bong-calorimeter notion of obesity didn’t pay proper respect to the complexity that is biology’s black box
  • I contend that the ‘meat sweats’ that may ensue after a large steak dinner, for example, makes clear that there are macronutrients specific consequences manifest in our endocrine and metabolic systems ⇒ surely that should suffice to cast doubt on the the Calories In Calories Out (CICO) view of obesity
  • Dr.Bikman’s family breakfast motto is ‘Come for the bacon and stay for the eggs’. Should this be Break Nutrition’s tagline?
  • I ask Dr.Bikman what is emerging in the LCHF/keto community that most interests or worries him
    • He’s disappointed in people’s reluctance to acknowledge, or even being openly hostile to, new research on alternative theories to the Somatic Mutation Theory (SMT) of cancer
    • He’s encouraged by oncologists trying to extract therapeutic benefit from lifestyle interventions like ketogenic diets


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