The emergence of GLP-1 receptor agonists (GLP-1 RAs) like semaglutide and tirzepatide has redefined the landscape of obesity treatment. Unlike earlier weight loss medications that primarily worked through central appetite suppression or sympathetic activation—often with concerning cardiovascular or psychiatric side effects—GLP-1 RAs engage a physiological system already integral to metabolic homeostasis.

GLP-1 is an incretin hormone secreted by intestinal L-cells in response to food intake. It enhances insulin secretion, inhibits glucagon release, slows gastric emptying, and promotes satiety. Newer GLP-1 drugs are more stable and have extended half-lives, allowing weekly dosing and more sustained physiological effects. Tirzepatide, for example, combines GLP-1 and GIP receptor agonism, enhancing both insulin sensitivity and lipid metabolism. These mechanisms contribute not only to weight loss but also to improved glycemic control, reduced cardiovascular risk, and better outcomes in conditions like NAFLD and PCOS.

Crucially, these medications impact long-term metabolic outcomes by addressing both energy intake and glucose utilization. Patients on GLP-1 therapies often exhibit reductions in visceral adiposity, decreased inflammatory cytokines, and improved lipid profiles—factors tightly linked to cardiometabolic risk.

However, this progress brings a new layer of complexity. While total body weight decreases, GLP-1 therapies do not selectively target fat mass. Without intervention, a portion of weight lost comes from lean tissue, including muscle. The downstream effect on resting metabolic rate, frailty, and physical resilience is still being actively studied. This highlights the need for tools to monitor not just “how much” weight is lost, but what kind of weight is lost.

2. What clinical or real-world data supports the effectiveness of GLP-1 therapies in preserving lean muscle mass, and where do the current gaps remain in monitoring muscle health during treatment?

Preserving lean muscle mass during weight loss is critical, especially in older adults or those with existing sarcopenia. Clinical data show that GLP-1 RAs do not inherently protect against muscle loss—in fact, like many weight-loss interventions, they can reduce both fat and lean mass.

In the STEP 1 trial, participants on semaglutide lost an average of 14.9% of their body weight over 68 weeks, but further body composition analysis revealed that about 39% of that weight loss came from lean mass. Similar patterns were observed in the SURMOUNT-1 trial with tirzepatide. This is clinically significant, as lean mass is a key determinant of metabolic rate, physical function, and long-term weight maintenance.

Real-world evidence reflects these findings. In clinical practice, patients on GLP-1 RAs who do not concurrently engage in resistance training or ensure adequate protein intake may see a decline in functional strength. However, most prescribing physicians are not equipped with tools to monitor these changes beyond anecdotal reports or delayed clinical markers such as sarcopenia or falls.

This is a critical gap in the standard of care. Current monitoring tools like DXA and MRI are expensive, time-consuming, and rarely integrated into primary or endocrinology care settings. Bioimpedance is more accessible but less reliable. No scalable, non-invasive solution exists to track muscle preservation longitudinally and dynamically—yet this is precisely what’s needed as millions more patients start GLP-1 therapy.

3. Could you elaborate on the development and validation of the novel protein biosensor—what makes it suitable for detecting early signs of muscle degradation in patients undergoing GLP-1 therapy?

At Biolinq, we’re developing a next-generation biosensing platform that combines the power of continuous molecular monitoring with the practicality of skin-wearable technology. Our proprietary electrochemical protein biosensor is designed to measure key biomarkers from interstitial fluid—the layer just beneath the skin—with high sensitivity, specificity, and temporal resolution.

Muscle degradation involves a cascade of biochemical events, including protein catabolism, inflammation, and shifts in amino acid metabolism. We've focused our sensor development on markers like creatine kinase (CK), myostatin, and muscle-specific troponins, which serve as early indicators of muscle breakdown. We are also exploring novel biomarkers such as 3-methylhistidine and branched-chain amino acid ratios that may offer even more refined insights.

What makes our sensor suitable for this application is threefold:

1. Non-invasive and continuous – Unlike blood draws, our platform collects data passively over hours or days, giving a dynamic picture of muscle health.

2. Sensitive to subtle changes – Early muscle degradation often happens before there’s a noticeable change in strength or mass. Our technology can detect these early shifts, enabling intervention before irreversible loss occurs.

3. Scalable and wearable – The device is designed for real-world use—lightweight, wireless, and discreet—so it can be integrated into patients’ daily lives without burden.

Our validation process includes both in vitro testing of target specificity and human pilot studies assessing biomarker correlation with exercise-induced muscle stress, dietary intake, and pharmacological intervention. We’re also working with metabolic disease researchers to co-develop digital endpoints for muscle health that can complement traditional metrics like weight or glucose.

4. How do you envision the integration of continuous biosensing technology, like the protein sensor, within the existing therapeutic workflow for obesity and metabolic disease management?

We envision biosensing technology serving as a central node in the therapeutic workflow—not just as a monitoring tool, but as an active agent in personalized, preventive care.

Let’s imagine a patient initiating GLP-1 therapy. Today, they receive a baseline metabolic panel, general dietary advice, and a follow-up visit in 4–12 weeks. With our sensor, this timeline shifts. Within the first week of treatment, the device can provide:

• A baseline of muscle-related biomarker trends

• Feedback on how well the patient is retaining lean mass

• Alerts if catabolism markers rise too sharply, suggesting poor protein intake or overmedication

Over time, this continuous data can be layered into existing platforms such as EHR systems or digital coaching apps. For providers, this means earlier, more targeted interventions—adjusting dose, recommending resistance exercise, or collaborating with nutritionists. For patients, it means real-time feedback, empowerment, and motivation.

We believe the future of obesity and metabolic disease management must move beyond episodic care. Continuous biosensing makes it possible to build adaptive, responsive treatment frameworks that evolve with the individual—not just the protocol.

5. As GLP-1 RAs become more widely adopted, what role will personalized data—such as muscle composition tracking—play in tailoring dosages, monitoring progress, and preventing adverse effects over time?

Personalized data is the future of precision obesity care. In the era of GLP-1 RAs, we’re not just treating excess weight—we’re treating a chronic, multifactorial metabolic disease with individualized manifestations. Muscle composition is one of the most underappreciated dimensions of this disease state, and its tracking will be vital for multiple reasons:

1. Tailoring dosages – Some patients respond rapidly to GLP-1 therapy and may benefit from dose reduction to prevent over-medication and preserve muscle mass. Others may need higher doses or adjunct support to achieve metabolic goals. Continuous biosensor feedback provides a physiological basis for those decisions—not just weight on a scale.

2. Preventing adverse effects – Muscle loss increases fall risk, reduces immune resilience, and undermines long-term independence. If we can identify early trends toward catabolism, providers can intervene before these effects manifest clinically.

3. Optimizing combination therapy – As more combination therapies emerge (GLP-1/GIP, GLP-1/glucagon, SGLT2 inhibitors), personalized biosensing will help determine which combinations offer the best balance of fat loss and muscle preservation for a given patient.

4. Long-term patient engagement – Personalized data turns passive patients into active participants. When individuals can see how their behavior—protein intake, physical activity, even sleep—affects their underlying physiology, adherence improves.

This data-driven approach also opens doors for research. By collecting high-resolution biomarker trends across thousands of patients, we can better understand the biological variability in response to GLP-1 therapy, stratify patients by risk, and design smarter interventions.

We are at an inflection point in metabolic health. GLP-1 receptor agonists have finally provided a tool that works for many people where lifestyle interventions alone fell short. But with this power comes responsibility—to monitor not just weight, but the quality of that weight loss; to prioritize healthspan, not just slimness.

At Biolinq, we believe that biosensing is the next essential layer in this paradigm. Our protein sensor is not just about detecting change—it’s about enabling a new kind of care: proactive, precise, and personal. We’re committed to closing the gap between drug effect and physiological feedback, empowering both patients and clinicians to make better decisions, every day.

As the field of obesity care continues to evolve, our goal is to ensure that metabolic success doesn’t come at the cost of muscle, function, or quality of life. We’re excited to work alongside partners, providers, and patients to make that future a reality.

Chaitrali Gajendragadkar

chaitrali.gajendragadkar@mmactiv.com

Senior Officer - Media Integrations

MedTech Spectrum

www.medtechspectrum.com