In this episode of The Metabolic Classroom, Dr. Ken Berry and Dr. Ben Bikman discussed the critical role of endogenous insulin, the limitations of focusing solely on glucose levels, and the implications of common markers like A1C and uric acid in understanding metabolic health.

Dr. Berry began by highlighting how many primary care physicians misunderstand the function of beta cells in type 2 diabetes, often believing that these cells “burn out” and stop producing insulin. Dr. Bikman clarified that in true type 2 diabetes, beta cells do not fail entirely; instead, insulin production often remains high or slightly decreases, which is still significantly higher than normal.

The problem lies in the body’s insulin resistance, not a lack of insulin production. Dr. Bikman emphasized the importance of measuring fasting insulin levels early in a patient's metabolic health journey, noting that levels above 6 microunits/mL can indicate potential problems.

The conversation then shifted to the A1C test, a common marker used to assess blood glucose levels over time. Dr. Berry and Dr. Bikman discussed the limitations of A1C, particularly how it can be falsely elevated or decreased based on the lifespan of red blood cells. Longer-lived red blood cells can cause a falsely high A1C, even if glucose levels are normal, while short-lived red blood cells can lead to a falsely low A1C in the presence of hyperglycemia. Dr. Bikman suggested that while A1C has value, it should not be the sole marker for assessing metabolic health. He also pointed out that A1C does not account for the glycation caused by other sugars like fructose, which can lead to significant damage not reflected in A1C results.

Dr. Berry raised concerns about the carnivore community, where some individuals see their A1C levels rise despite a healthy diet. Dr. Bikman explained that this could be due to longer-lived red blood cells resulting from a nutrient-rich diet. He recommended the fructosamine test as a better indicator of glucose glycation in these cases. The discussion also touched on the lack of tests for fructose and galactose glycation, leaving healthcare providers blind to the potential damage caused by high fructose intake, especially from fruit juices.

The classroom discussion concluded with an exchange about uric acid, particularly its relationship with fructose metabolism. Dr. Bikman shared insights from his research showing that uric acid, which is produced during fructose metabolism, can contribute to insulin resistance and inflammation. However, he also noted that ketones, produced during a ketogenic diet, can inhibit the inflammation caused by uric acid, providing a potential explanation for why individuals on ketogenic diets may experience improved metabolic health despite elevated uric acid levels.

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Learn more about Dr. Ken Berry: https://www.drberry.com/about

#InsulinResistance #Type2Diabetes #DrBenBikman #DrKenBerry #A1CTest #FastingInsulin #UricAcid #CarnivoreDiet #Fructose #MetabolicHealth #KetogenicDiet #Inflammation #BetaCells #Endocrinology #BloodGlucose #ProperHumanDiet #HealthLecture #MetabolicClassroom #BiomedicalScience #InsulinIQ

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In this episode of The Metabolic Classroom, Dr. Ben Bikman explores the metabolic effects of estrogens, particularly their role in glucose metabolism.

Estrogens, mainly produced in the gonads, play a crucial role in regulating blood glucose by enhancing insulin sensitivity. Dr. Bikman explained that estrogens improve insulin signaling through pathways such as PI3 kinase and AKT, which are essential for glucose uptake in muscle and fat tissues. Additionally, estrogens activate AMP-activated protein kinase (AMPK), further promoting glucose uptake and maintaining healthy blood glucose levels.

Estrogens also suppress glucose production in the liver by inhibiting key enzymes involved in gluconeogenesis, helping to prevent excess glucose release into the bloodstream. In contrast, progesterone decreases insulin sensitivity and promotes insulin resistance, counteracting some of estrogen's beneficial effects. This hormonal interplay affects glucose metabolism during the ovarian cycle, with estrogen-dominant phases being more favorable for glucose control.

During menopause, the significant drop in estrogen levels leads to increased insulin resistance and shifts in fat storage, often resulting in more central fat accumulation. While hormone replacement therapy (HRT) can mitigate some of these changes, it comes with risks that need careful consideration. Ben emphasizes the significant role of estrogens in glucose metabolism and their broader impact on metabolic health, especially in women.

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01:19 - Overview of Estrogens and Progesterone

02:20 - Cholesterol as the Precursor to Sex Hormones

03:34 - The Role of Aromatase in Estrogen Production

04:32 - Understanding the Family of Estrogens

05:56 - Estrogens and Glucose Metabolism: Key Signaling Pathways

06:54 - Insulin Signaling Pathway Overview

08:57 - How Estrogens Enhance Insulin Sensitivity

10:04 - The Role of AMPK in Glucose Uptake

12:11 - Estrogens' Dual Mechanism in Regulating Glucose Levels

13:18 - The Impact of Estrogens on Liver Glucose Production

15:33 - Estrogens' Role in Suppressing Gluconeogenesis

17:07 - Why Women Have Lower Risk of Type 2 Diabetes

19:28 - Metabolic Effects During the Ovarian Cycle

21:54 - Progesterone’s Influence on Insulin Resistance and Fat Storage

25:16 - The Shift in Fat Storage Patterns Post-Menopause

26:16 - Hormone Replacement Therapy: Metabolic Considerations

PI3K activation leads to the phosphorylation of Akt, a key protein in glucose metabolism, which promotes the translocation of GLUT4 (glucose transporter type 4) to the cell membrane, facilitating glucose uptake into muscle and adipose tissue: https://www.sciencedirect.com/science/article/pii/S155041311930138X?via%3Dihub

AMPK acts as an energy sensor and helps maintain cellular energy balance, which is crucial in regulating glucose and lipid metabolism: https://link.springer.com/article/10.1007/s12013-015-0521-z

Progesterone increases blood glucose levels by enhancing hepatic gluconeogenesis. This effect is mediated by the progesterone receptor membrane component 1 (PGRMC1) in the liver, which activates gluconeogenesis pathways, leading to increased glucose production, especially under conditions of insulin resistance: https://www.nature.com/articles/s41598-020-73330-7

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Dr. Ben Bikman, a biomedical scientist and professor of cell biology, discusses the phenomenon of anabolic resistance.

Anabolic resistance, primarily a problem associated with aging, refers to the reduced ability of muscles to synthesize protein in response to anabolic stimuli, such as protein intake and resistance exercise. This condition leads to a decline in muscle mass and function over time, contributing to a loss of physical capacity, increased risk of falls, and a greater dependency on others for daily living.

Dr. Bikman emphasizes the importance of muscle mass for overall health. Beyond physical function, muscle plays a crucial role in metabolic regulation, particularly glucose metabolism and insulin sensitivity. Muscle acts as a “glucose sink,” helping to regulate blood glucose levels and maintain insulin sensitivity. Therefore, maintaining muscle mass is vital for preventing metabolic disorders and enhancing longevity and health span.

Anabolic resistance is influenced by various age-related factors, including hormonal changes, reduced physical activity, insufficient protein intake, and chronic illnesses such as insulin resistance. The key intracellular signal involved in muscle protein synthesis is the mTOR1 pathway, which becomes less responsive with age and insulin resistance. Dr. Bikman also discusses the controversial use of rapamycin, a drug promoted by some longevity enthusiasts, which can inhibit mTOR1 and potentially exacerbate anabolic resistance and insulin resistance.

To combat anabolic resistance, Dr. Bikman highlights the importance of dietary and exercise interventions. Older adults require higher protein intake, particularly high-quality protein sources rich in leucine, to stimulate muscle protein synthesis effectively. Additionally, resistance exercise is crucial, with a focus on going to muscle fatigue to promote maximal muscle protein synthesis. Dr. Bikman stresses the need for older adults to prioritize resistance exercise over aerobic exercise to maintain muscle mass and function.

Dr. Bikman concludes by emphasizing the societal benefits of maintaining muscle mass and combating anabolic resistance. Strong, healthy, and independent individuals contribute to stronger communities and reduced economic burdens. By adopting proper dietary and exercise habits, individuals can improve their muscle health, enhance their quality of life, and increase their longevity.

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01:08 - Defining Anabolic Resistance

02:15 - Impact of Aging on Muscle Protein Synthesis

03:15 - Role of Anabolic Stimuli in Muscle Growth

05:15 - Risks Associated with Loss of Muscle Mass

06:17 - Muscle's Role in Metabolic Health

07:19 - Muscle Mass and Longevity

10:24 - Age-Related Factors: Hormones and Physical Activity

11:10 - Biochemical Signaling and mTOR1 Pathway

13:28 - Controversy Around Rapamycin and Longevity

15:43 - Rapamycin's Impact on Muscle and Testosterone

17:42 - Nutrient Sensing and mTOR1 Activation

18:40 - Importance of Leucine in Protein Synthesis

19:54 - Hormonal Regulation of mTOR1

20:55 - Consequences of Anabolic Resistance

21:52 - Combating Anabolic Resistance: Dietary Strategies

24:05 - Importance of High-Quality Protein Sources

26:05 - Role of Resistance Exercise in Combating Anabolic Resistance

28:55 - Exercise Protocols for Older Adults

30:55 - Importance of Resistance Exercise Over Aerobic Exercise

32:55 - Conclusion and Societal Benefits of Muscle Health

References:

Due to character length constraints, references are not posted here. For a complete list, please email: support@insuliniq.com with your request.

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Dr. Ben Bikman, professor of cell biology and metabolic scientist, delivers a lecture on the importance of fermentation and fermented foods from a metabolic perspective. He began by defining fermentation as the metabolic process where bacteria convert carbohydrates into organic molecules, emphasizing that bacteria primarily consume carbohydrates, not fats or proteins. Fermented foods such as dairy, vegetables, and beverages like kombucha and kefir are common examples. Fermentation not only changes the taste and texture of these foods but also has significant metabolic impacts.

A key benefit of consuming fermented foods is the reduction in glycemic load, which helps control blood sugar and insulin levels. Dr. Bikman highlightes studies showing that fermented milk improves glycemic control and lipid profiles in people with type 2 diabetes. He pointed out the importance of choosing genuinely fermented products, such as real sourdough bread, which lower postprandial glucose levels compared to conventional bread.

Dr. Bikman also discussed the production of short-chain fatty acids (SCFAs) during fermentation, such as acetate, propionate, and butyrate. These SCFAs have multiple health benefits, including improving gut health by maintaining gut barrier integrity, promoting an anti-inflammatory environment, and feeding gut cells. Additionally, SCFAs enhance metabolic functions, such as stimulating mitochondrial biogenesis and improving insulin sensitivity, which are crucial for overall metabolic health.

Fermented foods also provide probiotics when consumed raw and unpasteurized. These beneficial bacteria can help balance the gut microbiota, improve digestion, and support immune function. Dr. Bikman emphasizes the importance of incorporating raw, fermented foods into the diet to reap these probiotic benefits.

Lastly, Dr. Bikman introduced the concept of antinutrients, naturally occurring compounds in plant-based foods that can interfere with nutrient absorption. He explained that fermentation helps reduce the levels of antinutrients such as phytic acid, lectins, oxalates, and tannins, thereby enhancing the bioavailability of essential nutrients. He concludes by encouraging the incorporation of fermented foods into the diet as part of a strategy to control carbohydrate intake and improve metabolic health.

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01:00 – Overview of Fermentation

02:00 – Definition and Examples of Fermented Foods

04:00 – Benefits of Fermented Dairy: Kefir

06:00 – Fermented Foods and Glycemic Control

08:00 – Sourdough Bread vs. Conventional Bread

10:00 – Introduction to Short-Chain Fatty Acids (SCFAs)

12:00 – SCFAs and Gut Health

13:00 – SCFAs and Metabolic Benefits

15:00 – Probiotics in Fermented Foods

16:00 – Importance of Raw, Unpasteurized Fermented Foods

17:00 – Introduction to Antinutrients

18:00 – Examples of Antinutrients: Phytic Acid, Lectins, Oxalates, Tannins

20:00 – Fermentation's Role in Reducing Antinutrients

#FermentedFoods #MetabolicHealth #DrBenBikman #Fermentation #GutHealth #Probiotics #ShortChainFattyAcids #GlycemicIndex #InsulinResistance #Kefir #Sauerkraut #Kimchi #Kombucha #HealthyEating #NutritionScience #DiabetesManagement #AntiNutrients #HealthyGut #Mitochondria #InsulinIQ

My favorite meal-replacement shake: https://gethlth.com (discount: BEN10)

My favorite electrolytes (and more): https://redmond.life (discount: BEN15)

My favorite allulose source: https://rxsugar.com (discount: BEN20)

References:

(Due to character length constraints, references are not posted here. For a complete list, please email: support@insuliniq.com with your request.)

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In this episode of The Metabolic Classroom, Dr. Bikman introduces the concept of the Randle Cycle, also known as the glucose fatty acid cycle, in a lecture aimed at providing a better understanding of metabolism. The Randle Cycle, first identified by Dr. Philip Randle and his colleagues in the 1960s, explores how cells decide between using glucose or fatty acids for fuel. Dr. Bikman emphasized that this cycle has been misinterpreted on social media and aims to clarify its relevance in metabolic functions and nutritional decisions.

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00:00 - Introduction to the Metabolic Classroom and Dr. Ben Bikman

01:00 - Overview of the Randle Cycle (Glucose Fatty Acid Cycle)

02:00 - Historical Background: Philip Randle’s Research

03:00 - Experimental Model: Perfused Rat Hearts

04:00 - Key Terms: Glucose and Fatty Acids

05:00 - Concept of Substrate Competition

06:00 - Reciprocal Inhibition: Fats vs. Glucose

08:00 - Fatty Acid Oxidation Process

10:00 - Biochemical Pathways: Acetyl-CoA, NADH, and Pyruvate Dehydrogenase

12:00 - Role of Citrate in Glycolysis Inhibition

14:00 - Glucose Utilization and Malonyl-CoA

16:00 - Insulin’s Role in Fuel Selection

18:00 - Insulin’s Impact on Glucose and Fat Burning

20:00 - Diabetes Case Study: Type 1 and Type 2

22:00 - Type 1 Diabetes: High Glucose and Fatty Acids

24:00 - Ketones Production in the Liver

26:00 - Type 2 Diabetes: Insulin Resistance and Metabolic Inflexibility

28:00 - Insulin Resistance in Fat Cells

30:00 - Metabolic Inflexibility in Type 2 Diabetes

32:00 - Insulin Resistance in the Brain

34:00 - The Impact on Hunger and Neurological Disorders

36:00 - Conclusion: Importance of Insulin in Metabolic Health

#Metabolism #RandleCycle #DrBenBikman #InsulinResistance #GlucoseMetabolism #FattyAcidOxidation #MetabolicHealth #DiabetesResearch #Ketosis #Type1Diabetes #Type2Diabetes #InsulinRole #CellBiology #NutritionalScience #MetabolicFlexibility #Ketones #GlucoseUtilization #FatBurning #BiomedicalScience #HealthLecture

My favorite meal-replacement shake: https://gethlth.com (discount: BEN10)

My favorite electrolytes (and more): https://redmond.life (discount: BEN15)

My favorite allulose source: https://rxsugar.com (discount: BEN20)

References:

https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/randle-cycle

Insulin Regulation of Ketone Body Metabolism: https://onlinelibrary.wiley.com/doi/10.1002/0470862092.d0308

The Effects of a Ketogenic Diet and Exercise Interventions on Cognitive Function: https://faseb.onlinelibrary.wiley.com/doi/10.1096/fasebj.31.1_supplement.lb810

(Due to character length constraints, not every reference is posted above. For a complete list, please email: support@insuliniq.com with your request.)

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Dr. Ben Bikman’s lecture on leptin, delivered in his Metabolic Classroom series, highlights the hormone's critical role in metabolism. Leptin, primarily produced by white fat tissue, helps regulate energy balance by signaling the brain to suppress appetite and promoting mitochondrial biogenesis in muscle cells. Leptin levels correlate with body fat, and various factors like insulin and TNF alpha influence its production. Insulin significantly stimulates leptin secretion, highlighting a complex interplay between these hormones.

Leptin resistance, a condition where the body fails to respond effectively to leptin despite high levels, is similar to insulin resistance and often occurs in individuals with higher body fat. This leads to compromised satiety signals, energy expenditure, and potential obesity. Dr. Bikman also explores leptin’s broader effects on reproductive health, thyroid function, immune function, vascular health, and bone formation. These diverse roles underline leptin's significance in the body.

A historical perspective reveals leptin’s discovery in 1994 by Dr. Jeff Friedman’s lab at Rockefeller University. They found that leptin played a crucial role in regulating body weight in mice. However, leptin injections in obese humans did not yield similar results, as most obese individuals already have high leptin levels, leading to the understanding that leptin resistance, not a lack of leptin, is the issue in obesity.

The lecture concludes with practical insights on addressing leptin resistance, emphasizing the importance of controlling blood glucose and insulin levels, particularly through low-carb diets. This approach helps reduce leptin levels and improve leptin sensitivity, offering a pathway to better metabolic health and weight control.

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Professor Ben Bikman discusses sarcopenic obesity, a condition involving obesity and muscle loss. This condition results from factors like sedentary lifestyles, aging, and metabolic disturbances. While obesity is common, sarcopenia typically affects the elderly, diseased, or very sedentary individuals. The combination of excessive fat and muscle loss makes sarcopenic obesity particularly challenging.

Dr. Bikman explains the crucial role of muscle in blood glucose regulation. Muscle mass reduction impairs glucose control, leading to higher blood sugar levels and increased insulin resistance. Even a short period of bedrest can significantly reduce muscle mass and insulin sensitivity. Inflammation from enlarged fat cells also contributes to muscle loss and insulin resistance, creating a vicious cycle.

Insulin resistance and sarcopenic obesity can both cause and result from each other. Insulin resistance impairs muscle protein synthesis and promotes fat cell growth, leading to further insulin resistance. Reduced muscle mass and increased fat cell size negatively impact metabolic health. Bikman stresses the importance of diet in managing sarcopenic obesity, advocating for a low-insulin diet by controlling carbs, prioritizing protein, and not fearing fats.

To combat sarcopenic obesity, Dr. Bikman recommends proper nutrition and resistance training. Reducing insulin levels helps preserve muscle mass and promote fat loss. Resistance exercise is more effective than aerobic exercise for improving metabolic health. Consistent exercise and a controlled diet can help individuals manage or prevent sarcopenic obesity and improve metabolic health.

[01:02] Understanding Fat Cell Size

[02:07] Prevalence and Impact of Sarcopenic Obesity

[05:02] Role of Muscle in Glucose Regulation

[07:12] Effects of Bedrest on Muscle and Insulin Resistance

[10:43] Insulin's Role in Muscle Protein Synthesis

[16:04] Inflammation and Insulin Resistance

[20:43] Sarcopenic Obesity Contributing to Insulin Resistance

[24:41] Consequences of Sarcopenic Obesity

[26:32] Solutions: Diet and Exercise for Sarcopenic Obesity

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#MetabolicHealth #Sarcopenia #SarcopenicObesity #InsulinResistance #MuscleLoss #Obesity #HealthEducation #GlucoseControl #BloodSugar #InsulinSensitivity #MetabolicDisorders #HealthyAging #Inflammation #MuscleMass #FatLoss #NutritionTips #ExerciseScience #ResistanceTraining #LowCarbDiet #HealthTips #BenBikman #Metabolism #HealthyLifestyle #PreventDiabetes #FitnessEducation #DietAndExercise

Studies referenced found in YouTube show notes: https://youtu.be/iNmDbApK_FU

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In this episode of The Metabolic Classroom Dr. Ben Bikman focused on the effects of alcohol on insulin resistance, emphasizing how ethanol, the main form of alcohol, influences the brain and metabolism. He highlighted that alcohol is primarily metabolized by the liver and can cause insulin resistance through both direct and indirect mechanisms. Dr. Bikman detailed the molecular pathways by which ethanol inhibits insulin signaling, notably by disrupting the insulin receptor substrate (IRS1) and increasing oxidative stress, which impairs insulin's ability to regulate glucose.

Ben provided evidence from studies demonstrating ethanol's impact on insulin resistance at the cellular and whole-body levels. Research showed that ethanol consumption leads to higher insulin responses during glucose tolerance tests, indicating a reduced sensitivity to insulin. This phenomenon was observed in healthy humans who experienced a significant increase in insulin levels after consuming alcohol, suggesting a profound metabolic shift due to ethanol's presence.

The lecture also covered indirect effects of alcohol on insulin resistance. Many alcoholic beverages contain high amounts of sugar, exacerbating insulin and glucose responses. Alcohol disrupts sleep quality, leading to poor metabolic outcomes and increased cortisol levels, which further contribute to insulin resistance. Additionally, ethanol competes with other metabolic substrates, leading to fat accumulation in the liver and elevated glucose and fat levels in the body.

Dr. Bikman concluded by discussing the inflammatory response triggered by alcohol, particularly through the concept of a "leaky gut," where ethanol causes gaps in intestinal cells, allowing harmful substances like lipopolysaccharides (LPS) to enter the bloodstream and induce inflammation. This inflammation promotes ceramide production, further contributing to insulin resistance. Overall, Dr. Bikman emphasized the significant role of alcohol in metabolic health issues and encouraged mindfulness regarding alcohol consumption to mitigate these risks.

01:10 - Alcohol and Metabolism

02:18 - Direct Effects of Ethanol

03:26 - Insulin Receptor Disruption

06:38 - Whole-Body Impact

08:37 - Ceramides and Insulin Resistance

11:34 - Indirect Effects: Sugar

13:31 - Indirect Effects: Sleep

18:37 - Indirect Effects: Substrate Competition

23:34 - Inflammation and Leaky Gut

Studies Referenced:

(see notes on YouTube video: https://youtu.be/1aMuPTre1IU )

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