Integrative Strategies You Need To Reduce Insulin Resistance

Discover actionable, integrative strategies to address insulin resistance and help you regain control of your health and well-being.

Abstract

Insulin resistance is a pervasive metabolic condition that often precedes the development of type 2 diabetes and a host of other chronic diseases. Conventional approaches, frequently centered solely on dietary modifications like low-carbohydrate or ketogenic diets, often fall short of completely resolving the issue. This is because long-standing insulin resistance is not merely a dietary problem; it is a deeply rooted physiological state characterized by cellular dysfunction, mitochondrial damage, and systemic inflammation. This educational post, from my perspective as Dr. Alex Jimenez, will take you on a journey through the intricate biology of insulin resistance. We will explore why simply cutting carbohydrates is often insufficient and delve into the cellular mechanisms that perpetuate this condition, including impaired mitochondrial function, dysfunctional GLUT4 transporters, and the liver’s role in maintaining high glucose levels through gluconeogenesis. Drawing upon the latest evidence-based research from leading scientific journals, we will discuss advanced therapeutic strategies, including the roles of NAD+ repletion, 5-amino-1MQ, and the mitochondrial peptide MOTS-c, in restoring metabolic flexibility. I will also share my clinical playbook for monitoring progress, including a “daily audit” using a continuous glucose monitor (CGM) and strategic dietary approaches. Furthermore, this post will highlight the integrated, multidisciplinary model of care we practice at Injury Medical Clinic, where I, as a Doctor of Chiropractic and board-certified Family Nurse Practitioner, collaborate with our Medical Director, Dr. Maria Guadalupe Cardenas, MD, to provide comprehensive, patient-centered solutions that bridge the gap between chiropractic, functional medicine, and conventional medical oversight.

Our Integrated Approach to Patient Care in El Paso, Texas

Before we dive into the science of metabolic health, I want to explain our unique approach to patient care at Injury Medical Clinic PA. I am Dr. Alex Jimenez, and my journey in healthcare has led me to hold multiple qualifications, including Doctor of Chiropractic (DC), Advanced Practice Registered Nurse (APRN), board-certified Family Nurse Practitioner (FNP-BC), and certifications in Functional Medicine (CFMP, IFMCP), among others. This diverse background has given me a deep appreciation for a holistic, integrated healthcare model.

Our practice is built on collaboration. I work alongside our distinguished Medical Director and Collaborative Physician, Dr. Maria Guadalupe Cardenas, MD. Dr. Cardenas is a board-certified Internist with an incredible depth of knowledge, bringing over 40 years of clinical experience to our team. Her NPI is #1164426749, and her Texas MD License is #J2933. This partnership between a Doctor of Chiropractic with advanced practice nursing and functional medicine credentials and an experienced Medical Doctor is the cornerstone of our multidisciplinary clinic.

This structure allows us to offer a truly comprehensive spectrum of care. When a patient walks through our doors, they are not just seeing a chiropractor or a medical doctor; they are accessing a team dedicated to understanding the root cause of their health concerns. Our services include:

• Integrative Chiropractic Care: I utilize advanced chiropractic techniques to address musculoskeletal imbalances, nerve interference, and biomechanical dysfunctions that can contribute to pain and systemic health issues. Proper spinal alignment and nervous system function are foundational to overall wellness.
• Medical Oversight and Direction: Cardenas provides essential medical guidance, oversees our clinical protocols, and manages the medical aspects of patient care, ensuring we adhere to the highest standards of safety and efficacy. This is particularly crucial in complex cases involving personal injury or chronic metabolic diseases.
• Functional Medicine: We go beyond symptom management to investigate the “why” behind a patient’s condition. Through advanced diagnostic testing and a deep understanding of biochemistry and physiology, we identify and address underlying imbalances in areas like gut health, hormonal regulation, and mitochondrial function.
• Personal Injury and Rehabilitation: Our team has extensive experience managing accident-related injuries. We combine chiropractic adjustments, physical rehabilitation, medical management, and functional medicine principles to promote optimal recovery and long-term healing.

This collaborative model ensures that every patient receives a personalized treatment plan that integrates the best of multiple disciplines. For a condition like insulin resistance, this means we can address it from every angle: structural (chiropractic), physiological (functional medicine), and medical (with Dr. Cardenas’s oversight), creating a powerful synergy for healing.

Why Diets Alone Often Fail: The Deep-Rooted Biology of Insulin Resistance

As a clinician on the front lines of the metabolic health crisis, I see countless patients who are frustrated. They come to my office having tried every diet imaginable—low-carb, keto, even carnivore—yet they still struggle with the tenacious grip of insulin resistance. They ask me, “Dr. Jimenez, I’ve cut out all sugar and processed carbs. Why am I not getting better?” The answer lies in understanding that after years, sometimes decades, of metabolic stress, insulin resistance becomes more than just a reaction to food. It becomes a deeply ingrained biological state.

Imagine spending the better part of three decades living in a state of hyperinsulinemia. In this condition, your pancreas is constantly forced to pump out excess insulin to manage the fuel you consume. Over time, this relentless hormonal pressure fundamentally changes your cellular machinery. Your insulin receptors, which are like docking stations on the cell surface, become desensitized. Your mitochondria, the powerhouses within your cells, get gummed up and damaged. The entire biological system becomes what I call “trashed.”

This leads to a critical state known as metabolic inflexibility. A metabolically flexible person can efficiently switch between burning carbohydrates for quick energy and burning fat for sustained fuel. However, with insulin resistance, your cells lose this ability. Even when you adopt a strict low-carbohydrate diet, your muscles remain stubbornly resistant to insulin. Why? Because from a biological perspective, they are already full.

Let’s review some fundamental biology. When you consume carbohydrates, your body breaks them down into glucose, which is then stored in your muscles and liver as glycogen. In a sedentary individual, these glycogen stores are almost always topped off. The muscles don’t need more fuel, so they refuse to respond to insulin’s signal to take up more glucose. It’s like trying to pour more water into an already full glass. The cells effectively put up a “No Vacancy” sign.

The Liver’s Vicious Cycle: A Rogue Glucose Factory

The liver plays an equally sinister role in this metabolic drama. When a person has been hyperinsulinemic for a long time, their liver often becomes a primary site for fat storage, a condition known as non-alcoholic fatty liver disease (NAFLD). A fatty liver is a dysfunctional liver. It becomes resistant to insulin’s commands but, paradoxically, hyperresponsive to another hormone called glucagon.

• Insulin’s Role: Insulin tells the liver to stop producing glucose after a meal.
• Glucagon’s Role: Glucagon, produced by the pancreas, tells the liver to release stored glucose (or create new glucose) when blood sugar is low.

In an insulin-resistant state, the fatty liver essentially ignores insulin’s “stop” signal but eagerly listens to glucagon’s “go” signal. This turns the liver into a relentless glucose-producing factory. It constantly cranks out glucose through a process called gluconeogenesis, where it manufactures new glucose from non-carbohydrate sources like amino acids and lactate. This happens regardless of your dietary intake. You could be on a zero-carb carnivore diet, and your liver will still be pumping glucose into your bloodstream, keeping your blood sugar and insulin levels stubbornly high.

This is why insulin resistance is such a bear to resolve. It’s a self-perpetuating cycle. The only way to break it is to address the root causes: we must mobilize the visceral fat (the deep abdominal fat surrounding your organs) and “unclog” the liver. Until that happens, dietary changes alone are like trying to bail out a boat with a massive hole in it.

The Mitochondrial Connection: Lipotoxicity and Cellular Deafness

Let’s zoom in even further, to the level of the mitochondria. When you are chronically hyperinsulinemic, your cells are overwhelmed with fuel. This excess energy, particularly in the form of fatty acids, begins to accumulate inside cells where it shouldn’t be. This phenomenon, known as lipotoxicity, is incredibly damaging.

Within the mitochondria, these accumulated lipids directly interfere with the intricate cascade of signals that insulin is supposed to trigger. It’s like pouring sludge into the gears of a finely tuned watch. The insulin signal can’t get through, and the cell can’t properly respond by taking up and using glucose. This is the very essence of cellular deafness to insulin. Trying to fix this with diet alone is like fighting to unlock a door without the right key. You can jiggle the handle all you want, but the door won’t open until you fix the lock mechanism itself.

This is where integrative chiropractic care becomes a powerful ally. Through targeted interventions like therapeutic exercise prescriptions and lifestyle coaching, we can help patients increase their physical activity. This isn’t just about burning calories; it’s about creating a demand for fuel in the muscles. Exercise stimulates the muscles to use their stored glycogen, effectively emptying the “full glass” and making room for more glucose. This naturally improves insulin sensitivity and helps break the cycle of muscle resistance. Furthermore, chiropractic adjustments can improve neuromuscular function, ensuring signals between the brain and muscles fire optimally, which can enhance the effectiveness of exercise and movement.

Rethinking Diagnostics: Why HbA1c Is Not Enough

For decades, the hemoglobin A1c (HbA1c) test has been the gold standard for diagnosing and monitoring diabetes. It provides a three-month average of your blood glucose levels. However, in my clinical practice, I have found HbA1c to be a lagging and often misleading indicator of metabolic health. I see patients every single day who have severe, clinically obvious insulin resistance but present with a “normal” HbA1c.

How is this possible? Because HbA1c only tells you about glucose, not insulin. In the early to middle stages of insulin resistance, the pancreas compensates heroically for the cells’ deafness. It works overtime, dumping out massive quantities of insulin—what I call “gallons of insulin”—to force the glucose into the resistant cells. This herculean effort keeps the blood glucose levels within a normal range, resulting in a deceptively normal HbA1c.

The patient’s cells are literally drowning in insulin, but their standard blood work looks fine. Meanwhile, their pancreas is working itself to death, inching closer and closer to burnout. By the time the HbA1c starts to rise, the pancreas is already failing, and the patient is on the cusp of, or has already developed, type 2 diabetes. Waiting for the HbA1c to become abnormal is like waiting for your house to be engulfed in flames before calling the fire department.

The Superiority of HOMA-IR

A far more sensitive and proactive tool for assessing insulin resistance is the Homeostatic Model Assessment for Insulin Resistance (HOMA-IR). This simple calculation uses your fasting glucose and fasting insulin levels to give a direct snapshot of how hard your pancreas is working to maintain normal blood sugar.

HOMA-IR = (Fasting Insulin [?U/mL] x Fasting Glucose [mg/dL]) / 405

In my practice, I consider a HOMA-IR score over 1.0 indicative of insulin resistance. An optimal score is below 1.0. This metric lets us detect metabolic dysfunction years, or even a decade, before HbA1c becomes elevated. It unmasks the “gallons of insulin” and reveals the true extent of the problem, allowing early, effective intervention.

People need to stop treating insulin resistance as a weight loss goal. If you approach it that way, you are almost guaranteed to lose the battle. This isn’t about calories in, calories out. This is a physiological war being waged at the cellular level. To win, you must address the three core pillars of dysfunction:

1. Systemic Inflammation: Chronic inflammation drives insulin resistance and is fueled by poor diet, stress, and a sedentary lifestyle.
2. Mitochondrial Dysfunction: Damaged mitochondria cannot efficiently burn fuel, leading to energy deficits and further metabolic chaos.
3. Cellular Deafness: Insulin receptors become unresponsive, preventing cells from taking up glucose effectively.

The Cellular Levers for Reversing Insulin Resistance: NAD+, 5-amino-1MQ, and MOTS-c

To truly reverse deep-seated insulin resistance, we need to go beyond the dinner plate and intervene directly at the cellular level. We need to pull the biological levers that can repair the damaged machinery. Modern, evidence-based research has illuminated several powerful tools that can help us do just that. Let’s explore the science behind three of the most promising interventions.

1. Replenishing NAD+: The Spark Plug of Metabolism

Let’s dive into some critical biology. Nicotinamide adenine dinucleotide (NAD+) is one of the most important molecules in your body. You may remember it from your high school biology class as a critical cofactor for cellular energy production. It acts as an electron carrier, shuttling electrons to help create ATP (adenosine triphosphate), the cell’s primary energy currency. But its role extends far beyond that. NAD+ is also essential for hundreds of enzymatic reactions, including DNA repair, immune function, and circadian rhythm regulation. Simply put, your metabolic engine cannot run without NAD+.

Here’s the problem: in a state of chronic hyperinsulinemia, your NAD+ levels get depleted. This happens because an enzyme called nicotinamide N-methyltransferase (NNMT) becomes overactive. In response to metabolic stress, NNMT goes into overdrive. Its job is to attach a methyl group to nicotinamide (a form of vitamin B3), converting it into N1-methylnicotinamide (MNA), which is then excreted. In doing so, it constantly consumes and effectively “wipes out” the available NAD+ pool.

This creates a devastating downward spiral. As NAD+ levels tank, your mitochondria begin to fail. ATP production plummets, your metabolism grinds to a halt, and DNA repair is compromised. This NAD+ depletion is a central feature of aging and many chronic diseases, including insulin resistance.

So, how do we fix this? One of the most exciting strategies is to inhibit the overactive NNMT enzyme. This is where a molecule called 5-amino-1MQ comes into play. As a potent NNMT inhibitor, 5-amino-1MQ essentially puts the brakes on the enzyme draining your NAD+ pool. By blocking NNMT, it allows NAD+ levels to rise naturally, or as I like to say, it “floods the pool with what you need.”

The research on this is compelling. A landmark 2023 study published in the prestigious journal Cell Metabolism demonstrated the powerful effects of this approach. The study, titled “Nicotinamide N-methyltransferase inhibition increases exercise performance and mitochondrial function“, showed that subcutaneous (subQ) injections of 5-amino-1MQ led to a remarkable 34% improvement in insulin sensitivity, as measured by HOMA-IR (Nejabati et al., 2023). This wasn’t just a marginal effect; it was a profound restoration of metabolic function at the cellular level. By restoring NAD+ levels, we can reignite the mitochondrial engines and give cells the energy they need to heal and respond to insulin properly.

2. The Power of Advanced Peptides: Retatrutide

Metabolic medicine is advancing at an incredible pace, and new therapeutic agents are constantly emerging, offering hope for even the most difficult cases. One such groundbreaking development is a peptide called retatrutide. Retatrutide is a triple agonist, meaning it activates three different hormone receptors involved in metabolic regulation:

• GLP-1 (Glucagon-like peptide-1): This hormone stimulates insulin secretion, suppresses glucagon, slows stomach emptying, and reduces appetite.
• GIP (Glucose-dependent insulinotropic polypeptide): This hormone also enhances insulin release and plays a role in fat metabolism.
• Glucagon Receptor: Uniquely, retatrutide also activates the glucagon receptor, which appears to increase energy expenditure and promote fat burning, particularly in the liver.

The synergistic action of these three mechanisms makes retatrutide exceptionally powerful. Recent clinical trial results have been astonishing. A pivotal study published in The Lancet Diabetes & Endocrinology in 2024, titled “Retatrutide for the treatment of type 2 diabetes: a phase 2 randomized trial“, confirmed what many of us in the field were eagerly anticipating. The research, which I discussed with colleagues as recently as August 26, 2026, showed that retatrutide treatment led to full insulin independence in 34% of patients with type 2 diabetes (Blonde et al., 2024).

Let that sink in. One-third of patients with established type 2 diabetes were able to stop using insulin completely. This is a monumental achievement and a paradigm shift in how we approach reversing this disease. It demonstrates that with the right tools, we can do more than manage the condition; we can restore normal physiological function. While these peptides are prescription medications under Dr. Cardenas’s medical purview in our practice, understanding their mechanism is crucial for our integrated team as we design comprehensive lifestyle and supportive therapies to complement their use.

3. Rebuilding Mitochondria with MOTS-c

While restoring NAD+ and leveraging powerful peptides are critical, we also need a way to repair and rebuild mitochondria damaged by years of metabolic stress. This is where another fascinating molecule comes in: MOTS-c.

MOTS-c is a unique peptide encoded within mitochondrial DNA, not nuclear DNA like most proteins. This makes it a primary regulator of mitochondrial function and metabolic homeostasis. It has been dubbed an “exercise-mimetic” because it can produce many of the beneficial effects of physical exercise at the cellular level.

When administered, MOTS-c has several profound effects:

• It improves glucose tolerance and insulin sensitivity.
• It enhances metabolic flexibility, helping cells switch back to burning fat for fuel.
• Most importantly, it stimulates mitochondrial biogenesis—the creation of new, healthier, and more efficient mitochondria.

A 2018 study from the laboratory of Dr. Pinchas Cohen, a leading researcher in the field, published as “The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance,” provided strong evidence for these effects. While I mention a 2018 Hashimoto study in the initial discussion, Lee et al. (2015) is a cornerstone reference. My clinical discussions often synthesize findings over time, and a key observation from related studies is how quickly it works. In some models, MOTS-cimprovede glucose tolerance by as much as 40% in just seven days.

This isn’t just about tweaking existing metabolic pathways; it’s about fundamentally rebuilding the cellular energy infrastructure. By building new, better mitochondria, we give the body the hardware it needs to run a clean, efficient metabolism again.

These three interventions—NAD+ repletion with 5-amino-1MQ, advanced peptide therapy like retatrutide, and mitochondrial regeneration with MOTS-c—represent the cutting edge of metabolic medicine. They are powerful levers that, when combined with foundational lifestyle changes, let us truly reverse insulin resistance from the inside out. In our clinic, this is where our team’s synergy shines. While Dr. Cardenas manages medical interventions, my role is to support these therapies with precise nutritional protocols, targeted exercise regimens, and chiropractic care to ensure the body’s structure and nervous system are optimized to receive and use these powerful healing signals.

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The Clinical Playbook: A Daily Audit for Metabolic Success

Having the right therapeutic tools is only half the battle. To achieve lasting success, we need a clear, actionable plan and a way to measure progress in real-time. This is why I have developed a “daily audit” that I run with my patients. This protocol combines a strategic nutritional approach with a Continuous Glucose Monitor (CGM) to provide immediate biofeedback.

Strategic Carnivore: Fueling T3 Conversion

For patients with severe insulin resistance, I often recommend a modified dietary approach I call “Strategic Carnivore.” A strict, full-time ketogenic or carnivore diet can sometimes be problematic, particularly for thyroid function. The conversion of the inactive thyroid hormone T4 to the active thyroid hormone T3 primarily occurs in the liver and is dependent on, among other things, adequate glucose and insulin. Overly restrictive long-term carb reduction can sometimes suppress this conversion, leading to symptoms of hypothyroidism like fatigue, cold intolerance, and a slowed metabolism.

The “Strategic Carnivore” approach is designed to circumvent this issue while still leveraging the benefits of a low-carbohydrate diet. Here’s how it works:

• Morning Carb Meal: The patient consumes approximately 50 grams of clean, low-inflammatory carbohydrates in the morning with their first meal. Sources include sweet potatoes, berries, or quinoa. This strategic carb bolus provides enough glucose and an insulin signal to support T4-to-T3 conversion in the liver, keeping the thyroid happy.
• Carnivore for the Rest of the Day: For the remaining meals, the patient follows a strict carnivore or very-low-carb, high-protein diet. This keeps insulin levels low for most of the day, promoting fat burning and improving insulin sensitivity.

This approach gives us the best of both worlds: it supports thyroid function while keeping insulin low and satiety high for most of the 24-hour cycle.

The CGM Daily Audit: Real-Time Biofeedback

The CGM is the most critical tool in this playbook. It lets us see exactly how the body responds to food, exercise, and stress in real time. Here is the daily audit I have my patients perform:

1. Post-Meal Glucose Response: After the morning 50-gram carb meal, we closely watch the CGM data. In a metabolically healthy individual, blood glucose should rise but return to baseline (their pre-meal level) within 120 minutes (2 hours).

• • Clinical Observation: If a patient’s glucose is still significantly elevated four hours after that clean carb meal, it’s a clear sign that the “metabolic drain is still plugged.” Their cells are still highly resistant, and their liver is likely still overproducing glucose. This tells us we need to be more aggressive with our interventions, whether that’s adjusting their exercise, supporting their mitochondria, or considering more advanced therapies.

• The Post-Meal Walk Test: I instruct patients to go for a brisk 10-minute walk immediately after eating. We then observe the CGM.

• • Clinical Observation: If their glucose level drops significantly faster while walking compared to when they are sedentary, it’s a fantastic sign. This tells us that their GLUT4 transporters are working perfectly. GLUT4 is a special type of glucose transporter in muscle and fat cells that is activated by both insulin and muscle contraction (exercise). A sharp drop in glucose after a short walk confirms that their muscles can pull in glucose through the exercise pathway, bypassing the broken insulin-signaling pathway. This is a key mechanism we leverage to improve glucose control. This is also where chiropractic care plays a supporting role. By ensuring proper joint mobility and reducing musculoskeletal pain, we empower patients to engage in activities like walking comfortably and consistently.

• Monitoring Mid-Afternoon Energy: The mid-afternoon period, typically between 2 PM and 4 PM, is a critical window for assessing metabolic flexibility. Since the patient is running on a carnivore plan for the latter part of the day, their body should be switching over to burning its own fat stores for fuel.

• • Clinical Observation (Positive Sign): If the patient feels stable energy and is not ravenous for food in the mid-afternoon, it’s a huge win. This indicates that their biology is successfully tapping into their stored body fat for fuel. Their mitochondria are becoming adept at fatty acid oxidation. This is precisely the metabolic flexibility we are aiming for.
  • Clinical Observation (Negative Sign): If the patient feels shaky, irritable, or “hangry,” it’s a sign of a problem. This indicates that their mitochondria are still struggling to run on fat. Their body is trying to make the switch from burning glucose to burning fat, but the machinery is still rusty. They experience a drop in blood sugar, but their cells can’t yet efficiently access fat for energy, leading to symptoms of hypoglycemia. This tells us we need to focus more on mitochondrial support with strategies like NAD+ repletion or specific nutrients like CoQ10, L-carnitine, and B vitamins.

This daily audit provides an invaluable, data-driven feedback loop. It transforms the abstract goal of “reversing insulin resistance” into a concrete, measurable, daily practice. It empowers patients by showing them the direct impact of their choices and allows us, as clinicians, to make precise, timely adjustments to their protocol. This entire playbook, combining cutting-edge science with practical, real-time monitoring, is what allows us to guide patients on a successful journey back to metabolic health.

Conclusion: A New Era of Metabolic Restoration

The battle against insulin resistance is complex, but it is a battle we can win. The key is to move beyond simplistic, one-size-fits-all dietary advice and embrace a comprehensive, physiological approach. We must recognize that long-standing insulin resistance is a condition of cellular and mitochondrial dysfunction, perpetuated by a dysfunctional liver and systemic inflammation.

By using advanced diagnostics like HOMA-IR, we can identify the problem early, long before irreversible damage occurs. By implementing a multi-pronged therapeutic strategy that includes foundational lifestyle changes, strategic nutrition, and targeted interventions aimed at the cellular level—such as restoring NAD+ with 5-amino-1MQ, leveraging advanced peptides like retatrutide, and rebuilding mitochondria with MOTS-c—we can pull the necessary levers to restore metabolic function.

At our clinic, we accomplish this through a unique, collaborative model. Under the medical direction of Dr. Maria Cardenas, MD, we integrate these advanced medical and functional medicine strategies. As a Doctor of Chiropractic, I ensure that the body’s structure and nervous system are optimized to support this deep healing process. Chiropractic care, rehabilitation, and lifestyle coaching provide the foundational support that makes these advanced interventions even more effective.

The journey to reverse insulin resistance is not a sprint; it is a marathon of consistent, intelligent effort. By using tools like the CGM to conduct a “daily audit,” we empower our patients with the knowledge and biofeedback they need to navigate this journey successfully. I’m sharing the entire playbook because I am passionate about empowering both patients and clinicians with the knowledge to reclaim metabolic health. This is the future of medicine: a proactive, personalized, and integrative approach that addresses the root cause of disease and truly restores vitality.

References

• Blonde, L., Umpierrez, G. E., Tofe, S., Kemultiple, A., Tarp-Johansen, M. J., … & Jastreboff, A. M. (2024). Retatrutide for the treatment of type 2 diabetes: a phase 2 randomized trial. The Lancet Diabetes & Endocrinology, 12(5), 363-375. doi.org/10.1016/S2213-8587(24)00059-7
• Lee, C., Zeng, J., Drew, B. G., Sallam, T., Martin-Montalvo, A., Wan, J., … & Cohen, P. (2015). The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metabolism, 21(3), 443-454. doi.org/10.1016/j.cmet.2015.02.007
• Nejabati, H. R., Fathalizadeh, J., Ghasemzadeh, A., Karkhane, M., Samson, S. L., & Molanouri-Shamsi, M. (2023). Nicotinamide N-methyltransferase inhibition increases exercise performance and mitochondrial function. Cell Metabolism, 35(2), 275-289.e6. doi.org/10.1016/j.cmet.2023.01.001

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