Gregory M. Weiss, M.D.

Diabetes remains one of the most significant health problems in the world. Substantial effort has been made to catch diabetes early and adhere to evidence-based practice in an effort to decrease the incidence of the disease and prevent a myriad of diabetes-related complications. Despite our best efforts as clinicians, the incidence of diabetes in the United States of America has not declined since 2000.

A prediabetic state has been recognized by the Centers for Disease Control and Prevention largely in an effort to intervene before clinical type 2 diabetes has developed. The goal of early recognition of those at risk for type 2 diabetes is to promote a healthy lifestyle through diet, exercise, and weight loss in the hopes of preventing or delaying clinical diabetes and the cardiovascular consequences of elevated blood glucose levels.

Eva Tseng, MD, MPH, assistant professor of medicine at Johns Hopkins, and colleagues recognized the disconnect between prediabetes screening by primary care providers and referrals to nutritionists and endocrinology specialists. As such, Tseng sought to examine the clinical care of prediabetic patients by primary care providers while determining what patient factors influence that care.

 The authors further hoped to understand why the rates of clinical type 2 diabetes have not gone down. Their results were published in the March 2nd edition of the Journal of General Internal Medicine.

The authors examined a large cohort of patients who met laboratory criteria for prediabetes defined as a Hemoglobin A1C between 5.7% and 6.4%.

 Tseng was surprised to find that only 13% of visits to primary care providers in this cohort were coded with prediabetes as a diagnosis.

 Only two-thirds of these patients were ordered follow-up glycemic testing.

 Only 1% of prediabetic patients were referred to a nutritionist and 5.4% started on metformin as treatment.2 Over the twelve months following entry into the cohort, 6% of subjects progressed to type 2 diabetes.

A disconnect clearly exists between initial laboratory studies and interventions that may in many cases be lifesaving in the long term.

“Our results show that we have considerable room to improve in the identification and care of people with prediabetes within our health system and likely in many other places across the United States,” Tseng noted. 

One sliver of good news is that, even though few prediabetic patients were coded as such, the ones that were and received referrals, saw a nutritionist and were prescribed metformin the twelve months after entering the cohort.

 While higher risk patients like those with high body mass indices, and higher glucose levels were more likely to be recognized and referred, they were also more likely to progress to type 2 diabetes in the subsequent year.2

Tseng believes that these results present an opportunity for more aggressive recognition of prediabetes and prompt intervention.

 Patients should be armed with information that may change the course of their health dramatically. This can only occur when prediabetes is recognized, and patients are informed of the basic steps they can take to prevent progression to type 2 diabetes. While medical interventions like metformin therapy can slow the progression to clinical diabetes, patients can do a lot on their own with the right guidance. Even low levels of exercise and small changes in diet can help slow or prevent worsening blood glucose levels and insulin resistance.

While these data are frustrating to clinicians and patients alike, they offer an opportunity to change. Complacency is the antithesis of progress. We cannot afford to be complacent where diabetes is concerned. The cardiovascular sequelae, loss of productivity, reduced quality of life, and costs associated with continued inaction are unacceptable.

The responsibility rests on us all but primary care providers, in particular, must recognize prediabetes, diagnose it, and make the appropriate referrals promptly. If appropriate, metformin should be started and regular laboratory screenings for blood glucose and HgbA1C performed. Those at higher risk should be followed closely and treated aggressively lest they progress to type 2 diabetes more quickly. With vigilance and persistence, we as clinicians can change the trajectory of our prediabetic patients and really make a difference in their lives.

Centers for Disease Control and Prevention. National Diabetes Statistics Report, 2020. Atlanta, GA: Centers for Disease Control and Prevention; 2020.

Tseng, E., MD MPH, Durkin, N., BS, Clark, J. M., MD MPH, et al. Clinical care among individuals with prediabetes in primary care: a retrospective cohort study. 

 (2022). https://doi.org/10.1007/s11606-022-07412-9

Articles

Dr. Gregory Weiss discusses prediabetes screening in the US as a method help quell the growing diabetes epidemic in younger populations.

Prediabetes: It’s Never Too Early to Connect the Dots, with Gregory Weiss, MD

Hypertension is one of the most common conditions in the world and is a significant risk factor for kidney disease, stroke, and cardiovascular disease. The primary pathophysiological feature seen with prolonged hypertension is a thickening of arterial walls which, over time, can lead to organ damage. 

Maria Luisa Sequeira-Lopez MD, a physician at the University of Virginia, has uncovered a peculiar association between the pathophysiology of hypertension and the long-term use of a ubiquitous class of blood pressure medications.

A primary target in the management of hypertension is the renin-angiotensin-aldosterone system (RAA). The RAA is primarily responsible for maintaining an adequate blood pressure such that organs are perfused and the organism in question is able to survive and function. The pathology of hypertension is linked to an overactive RAA system. As such angiotensin-converting-enzyme inhibitors (ACEi) were developed as a treatment for hypertension. These drugs prevent the conversion of angiotensin to its vasoconstricting form, angiotensin II. The peculiarity Sequeira-Lopez and colleagues found was that long-term use of ACEi’s lead to the same arteriolar thickening and organ dysfunction, in a mouse model and in humans, that long-term hypertension itself produced.

Sequeira-Lopez looked at mice with an ablated renin gene. What they found was a progressive thickening of the afferent arterioles and interlobular arteries in the mouse kidneys.

 Stranger still, the arteriolar thickening was due to an increase in renin cells within the walls.

 This same phenomenon was seen in human kidneys following extended inhibition of the RAA system.

 At closer examination it was found that the invasive renin cells were not the classic endocrine cells but of a matrix-secretory type that is pathological to kidney arterioles.1 In both cases, human inhibition of the RAA system or renin knock-out mice, invasion of the kidney arteriole by pathological renin cells led to reduced blood flow and ischemia.

These findings are both interesting from a basic science perspective and troubling from a clinical viewpoint. Drugs targeting the RAA system are the mainstay of many hypertension treatment regimens. In fact, ACEi’s and angiotensin receptor blockers (ARBs) are often employed to protect the kidneys in diabetic patients with and without hypertension. Not only are these drugs being used by millions of patients worldwide, they have also been shown to reduce the risk of developing major cardiovascular events including heart attacks, strokes, and death.

These conflicting findings present a bit of a dilemma. For Sequeira-Lopez’s part she does not advocate for discontinuation of ACEi or ARB treatments at this time. She does however call for prospective, randomized, controlled investigations aimed at defining the real-life implications of her findings. Ultimately, we as clinicians measure the effectiveness of our treatments based on outcomes. Even though these data indicate that drugs targeting the RAA system cause thickening of renal arterioles the fact that these drugs are associated with better survival and in most cases increased quality of life should be the driving factor. The role of basic science research is to determine what the figuratively microscopic factors are that produce our macroscopic clinical picture. Now that these authors have uncovered a potential problem with a trusted and proven hypertension treatment it will be up to others to examine the clinical implications in the short and long term.

With over a billion people suffering from hypertension worldwide this discovery warrants a closer look. How can it be that the very treatment produces the same pathological sequelae as the disease itself? It is not uncommon for a study to raise more questions than answers. This is the basis of discovery. By building on good science, we find answers and start asking more questions. With a fresh look at an old treatment, we see here that the book isn’t closed on RAA inhibition.

Watanabe, H., Martini, A. G., Sequeira-Lopez, M. L. S., et al. Inhibition of the renin-angiotensin system causes concentric hypertrophy of renal arterioles in mice and humans. 

Dusing R. Mega clinical trials which have shaped the RAS intervention clinical practice. 

Dr. Gregory Weiss provides perspective on recent data detailing the potential for kidney damage as a result of long-term inhibition of the renin-angiotensin system. 

Inhibition of the Renin-Angiotensin System and the Potential for Kidney Damage

Proper nutrition has been recognized globally across all medical specialties as a foundation for health and wellness. Nutrition or the lack of is often the cause of disease and can be modified or enhanced to treat disease. 

Whether it be reducing salt intake in patients with hypertension or heart disease or increasing calories and protein in malnourished patients, dietary modifications can be a key part of both prevention and treatment of disease. There exists no better example of a pathologic condition where nutrition has a large impact than kidney disease.

Kidney disease is a global problem of great magnitude. Some estimates put the global burden of kidney disease at close to one billion adults and this number appears to be increasing.

 There is broad agreement among clinicians that nutrition intervention is a key component in managing chronic kidney disease (CKD). Through proper nutrition, patients with CKD can have a higher quality of life and more years without depending on kidney replacement therapy (KRT), or dialysis, which is both costly and time-consuming.

 The key targets of nutritional therapy in CKD include: preventing protein-energy wasting, intervening early when protein-energy wasting occurs, and ameliorating cardiovascular risk factors related to CKD.

Knowing that nutrition is important is a good start, but evidence suggest that nutritional information is not getting to patients with CKD.

 Surveys conducted globally indicate that in addition to there being a shortage of dietitians able to provide nutritional education to patients with kidney disease, many of those patients receive either suboptimal or no support at all.

 Dr. Yee-Moon Wang and colleagues at the University of Hong Kong examined excerpts from the Global Kidney Health Atlas Team’s surveys. Specifically, Dr. Wang looked at surveys dealing with the current global availability, capacity, and cost of kidney nutrition services as well as the communication between nutritionists and kidney specialists. What they found was startling.

Less than half of the over 150 countries included had dietitians who specifically provide kidney nutrition support.

Communication between dietitians and kidney specialists was spotty at best.

Less than half of countries perform formal assessments of nutrition status for CKD patients.

Oral nutrition supplement availability varied widely from country to country.

Counseling by a trained nutritionist is not provided in almost two-thirds of low and lower-middle income countries and never available in almost one-quarter of low-income countries.

In an editorial Dr. Arpana Lyengar and Dr. Valerie Luyckx state,

“This global survey is an important wakeup call to countries across the income spectrum. (Further) It exposes gaps and concerns related to kidney nutrition care, serving up a plate full of food for thought, that must now be followed by action.”

One of the key findings of the study, significant heterogeneity between localities, regions, and countries, comes as no great surprise. There exist great disparities between health systems based on socioeconomic, geographical, and technological lines. The density of dietitians versus populations size can be a significant factor. Compounding the problem, it is often countries of low socioeconomic status where CKD rates are the highest. There is no quick solution to this problem.

The authors agree that assessment is a good place to start.

 As with most medical conditions, identification of those at risk is key. Once identified resources such as available dietitians and educational materials can be allocated, and connections made with renal specialists. Reducing a need for dialysis whether through preventative education or nutritional support in the form of supplements and or healthy food would reduce the global burden of CKD in terms of both quality of life and cost.

The authors of this study highlight the primary implication of these finding as a call to action to raise global awareness and the importance of kidney nutrition assessment and care.

They believe that increased global advocacy and a shift in governmental prioritization and allocation of funds toward a campaign designed to promote nutritional support for kidney disease will lead to better quality of life, a reduced need for dialysis, and in the long run, cost savings for the very communities making the investment in supporting the dietary needs of their citizens suffering from kidney disease.

Jager KJ, Kovesdy C, Langham R, Rosenberg M, Jha V, Zoccali C: A single number for advocacy and communication- worldwide more than 850 million individuals have kidney diseases. Kidney Int 96: 1048–1050, 2019

Yee-Moon Wang, A., Okpechi, I. G., Fen Ye, C.P. K., et al. Assessing global kidney nutrition care. CJASN 17: 38–52, 2022. doi: https://doi.org/10.2215/CJN.07800621

A recent study published in the Journal of the American Society of Nephrology suggests patients with chronic kidney disease have little access to reliable information related to nutrition for patients with chronic kidney disease.

Nutrition Information Hard to Find, Access for Patients with Kidney Disease 

This article was originally published on 

Cardiovascular disease (CVD) remains the leading cause of death in the world. This fact holds true for women as well as men.

 In the last two decades observational studies have noticed that the risk for coronary heart disease increases significantly following the transition into menopause.

While women generally develop coronary heart disease (CHD) later than men, a clear inflection point at midlife warranted an explanation. Studies looking for a reason for this increase in CHD risk discovered distinct patterns of alterations in endogenous sex hormones that resulted in adverse changes in body fat, lipids, and lipoproteins, as well as structural and functional measures of overall vascular health.

 These revelations have led the American Heart Association (AHA) to release a scientific statement addressing the implications of menopausal transitioning on CVD in women.

The last AHA guidelines addressing CVD prevention in women were released in 2011. In the time since then much more has been discovered about the complexities of the menopausal transition (MT) with major implications on CV risk for women in midlife. The primary hormonal changes experienced through the five stages of the MT involve estradiol and follicle-stimulating hormone levels. Typically, estradiol levels begin to fall before the final menstrual period while levels of follicle-stimulating hormone rise.

 While these changes may lead to the symptoms women experience during the MT, researchers have found that the symptoms themselves may herald ominous CV changes.

Symptoms women commonly experience during the MT include hot flashes and night sweats, mood changes, sleep and cognitive disturbances, genitourinary, and sleep function changes. Hot flashes and night sweats are examples of vasomotor symptoms that may occur in conjunction with higher body fat composition and are associated with cigarette smoking, depression and lower educational level.

 Vasomotor disturbances may also be responsible for some measure of increased CV risk.

Five characteristics of menopause have been found to influence CV risk. Studies have shown that women who experience menopause at less than 45 years of age experience exhibit significantly higher cardiovascular risk when compared to those who are older. Data from the Framingham Heart Study showed that earlier menopause was associated with increased CVD but also that high cholesterol, systolic blood pressure, and diastolic blood pressure led to earlier menopause.

 This points to a clear association between preexisting CV risk factors and the MT leading to decreased CV health.

The second characteristic is type of menopause. Some studies showed that the risk for CHD was higher if menopause was caused by surgical removal of the ovaries when no estrogen therapy was prescribed.5 This theory was modified when it was found that the timing of surgical menopause was important. Surgical removal of the ovaries at a young age increased the risk of CHD while removal at the time of normal menopause did not.

The third characteristic is the stage of menopause where it appears that the most deleterious changes in blood pressure and intima-medial arterial thickening occur during the later stages of menopause.

 Endogenous estradiol levels have also been shown to affect CV risk with higher levels being associated with lower progression of carotid narrowing over time.

Finally, the previously mentioned vasomotor symptoms of menopause correlate to reduced flow-mediated dilation and greater aortic calcification independent of other CVD risk factors or hormonal levels.

In addition to lifestyle behavior modification in the form of weight loss and smoking cessation, the evidence suggests a role for menopausal hormone therapy (MHT).

 It appears that initiating MHT before the age of 60 or within less than 10 years since menopause confers a CV risk-benefit while later initiation may increase risk.

 Treatment with MHT may also mitigate other comorbidities by promoting lean body mass and lower body mass index as well as decreased levels of fasting glucose. Once started stopping MHT increased the risk of CVD in menopausal women.

Finally, while data for primary and secondary prevention of atherosclerotic disease and improved survival with lipid-lowering interventions is lacking, there may be a role for such therapy during the MT.

It is clear that the MT is a uniquely impactful facet of a woman’s cumulative cardiovascular risk deserving of close attention. Clinicians need to recognize the changes that occur and armed with the knowledge in the scientific statement, educate patients, tailor interventions, and provide the treatment women need to navigate this unique time. Through encouragement of lifestyle changes, management of other risk factors for CVD, and patient-specific approaches to MHT women can realize increased quality of life, reduced CV risk, and potentially a longer and more satisfying life.

Benjamin EJ, Muntner P, Alonso A, Bittencourt MS, Callaway CW, et al; on behalf of the American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee. Heart dis- ease and stroke statistics—2019 update: a report from the American Heart Association [published correction appears in 

2019;139:e56–e528. doi: 10.1161/CIR.0000000000000659

Samar R. El Khoudary, Brooke Aggarwal, Teresa M. Beckie, et al. Menopause transition and cardiovascular disease risk: implications for timing of early prevention. A scientific statement from the American heart association. 

. 2020;142:00–00. DOI: 10.1161/CIR.0000000000000912

El Khoudary SR. Gaps, limitations and new insights on endogenous estro- gen and follicle stimulating hormone as related to risk of cardiovascular disease in women traversing the menopause: a narrative review. 

2017;104:44–53. doi: 10.1016/j.maturitas.2017.08.003

Muka T, Oliver-Williams C, Kunutsor S, Laven JS, et al. Association of age at onset of menopause and time since onset of menopause with cardiovascular outcomes, intermediate vascular traits, and all-cause mortality: a systematic review and meta-analysis. 

2016;1:767–776. doi: 10.1001/jamacardio.2016.2415

Colditz GA, Willett WC, Stampfer MJ, Rosner B, Speizer FE, Hennekens CH. Menopause and the risk of coronary heart disease in women. 

1987;316:1105–1110. doi: 10.1056/NEJM198704303161801

Hurston RC, Sutton-Tyrrell K, Everson-Rose SA, Hess R, Matthews KA. Hot flashes and subclinical cardiovascular disease: findings from the Study of Women’s Health Across the Nation Heart Study. 

2008;118:1234–1240. doi: 10.1161/CIRCULATIONAHA.108.776823

Dr. Gregory Weiss offers perspective on a recent guideline update from the American Heart Association outlining strategies to best manage risk of cardiovascular disease in women entering menopause. 

Physician Perspective: AHA Guidelines on Managing CVD Risk During Menopause

This year clinicians and researchers across all disciplines of medicine have witnessed many firsts. As we navigate a perilous landscape dominated by the global COVID-19 pandemic, we have seen an extraordinary adaptation in the academic community. Science, medicine, and humanity itself must go on.

In keeping with this idea, the American Heart Association (AHA) has just completed its first virtual annual meeting from which the global academic community has introduced the latest research and insight in the field of cardiovascular science. In light of the incredible strain the pandemic has had on the global economy we present four sessions from the AHA Scientific Sessions 2020 highlighting the cost versus benefit of the latest drugs that treat type II diabetes mellitus that are also known to reduce cardiovascular (CV) risk.

On November 13th, 2020, Joseph Azuri, MD, and colleagues from Tel Aviv, Israel presented, in session P2007, a comparison between empagliflozin, an inhibitor of the sodium-glucose cotransporter 2 (SGLT2) and oral semaglutide, the first oral glucagon-like peptide 1 (GLP-1) receptor agonist. In keeping with the AHA strategic goal of reducing cardiovascular mortality by 20% these two drugs have been shown to significantly reduce the incidence of CV mortality in patients with type 2 diabetes mellitus and known CVD.

In light of the potential cost burden adding a new drug to a diabetes treatment regimen creates, Azuri sought to determine which drug would be most cost-effective while still reducing CV risk in type 2 diabetics. The research team went on to calculate the cost needed to treat (CNT) and prevent one case of CV mortality using either drug. They found the annual costs for empagliflozin and semaglutide were $4,572 and $6,680, respectively.

 In light of the similarity between the drugs with regards to efficacy and CV risk reduction, Azuri’s team recommends empagliflozin as the more cost-effective treatment.

In a second session on November 13th, 2020, P2013, Azuri and colleagues went on to compare three popular GLP-1 receptor agonists. With regards to semaglutide, dulaglutide, and liraglutide, the American Diabetes Association recommends providing one of these GLP-1 therapies to patients with type 2 diabetes and established CVD regardless of glycemic control.

 Concerned about the staggering costs associated with these new drugs Azuri sought to compare the 3 drugs for cost-effectiveness.

Azuri again calculated the annual cost needed to prevent one major adverse cardiovascular event (MACE) utilizing each of the three drugs in patients with type 2 diabetes and established CVD. The relative costs were $557,000 for semaglutide, $1,179,360 for liraglutide and $1,605,904 for dulaglutide.2 The research team concluded that, for secondary prevention of MACE in patients with type 2 diabetes and established CVD, semaglutide provides more value than the other two medications.

In session P1146 on November 13th, a colleague of Azuri’s, Ronen Arbel, PhD, further breaks down the cost effectiveness of two different preparations of the GLP-1 drug semaglutide. With an oral preparation of semaglutide now available, Arbel imagined that patients may prefer it over a subcutaneous injection for prevention of MACE in patients with type 2 diabetes.

Following the previous model, Arbel calculated the average annual cost for both preparations needed to prevent one MACE. The research team found that the average costs per year were $641,823 and $855,040 for the subcutaneous and oral preparations respectively.

 They further looked at the cost relationship between the two preparations and the endpoints of MACE versus cardiovascular mortality (CVM) alone. They concluded that the subcutaneous preparation of semaglutide was more cost-effective for the prevention of MACE in patients with type 2 diabetes but that for the prevention of CVM the oral preparation provided a significantly better monetary value.

Finally, in session MP463, also on November 13th, Arbel and colleagues looked at the cost-effectiveness of icosapent ethyl, a prescription omega-3 fatty acid supplement known to aid in prevention of MACE in patients with hypertriglyceridemia. The team looked specifically at the difference in cost when used for secondary prevention in diabetic patients with known CVD and for primary prevention in those with risk factors for CVD.

Arbel analyzed the cost of icosapent ethyl to prevent one MACE per year when prescribed for either primary or secondary prevention. The average cost of icosapent ethyl annually was $874,500 versus $206,965 when used for primary and secondary prevention respectively.

 The team found that the cost needed to treat was four times higher in the primary prevention group when compared to the secondary prevention group concluding that prescribing icosapent ethyl for diabetic patients with known CVD is significantly more cost effective.

We as clinicians often overlook the cost of the therapies we prescribe focusing solely on the most effective and proven treatments for our specific patients. These reports show that, when given choices between equally efficacious treatments, cost can play a significant role in our decision making and should. Of final note, we should all consider the enormous monetary amounts reported above. Reread those annual costs and consider the relative burdens such numbers place on patients and the health care system overall. A discussion for another time.

In a recent column Gregory Weiss, MD, uses studies from AHA Scientific Sessions 2020 to compare the cost-effectiveness of antihyperglycemic agents for reducing cardiovascular events. 

Comparing Cost-Effectiveness of Antihyperglycemic Agents with Cardiovascular Benefit

Empagliflozin leads to substantial reductions in liver fat in patients with type 2 diabetes mellitus (T2DM).

Empagliflozin also leads to a significant decrease in the liver function test alanine aminotransferase (ALT).

Levels of aspartate aminotransferase (AST) and gamma-glutamyl transpeptidase (GGT) were also reduced, although not significantly with empagliflozin treatment in patients T2DM.

Non-alcoholic fatty liver disease (NAFLD) is a build up of fat on the liver, but not related to drinking alcohol.

Mabrish Mithal, MD, of Medanta-The Medicity Hospital in Delhi, India states, “NAFLD can progress to [non-alcoholic steatohepatitis, NASH], and subsequently to cirrhosis and even cancer of the liver, potentially fatal conditions. NAFLD is particularly common in diabetes. Medications to treat NAFLD/NASH are sorely needed.”

Empagliflozin is a sodium glucose cotransporter-2 (SGLT-2) inhibitor that has been shown in rodent models to reduce liver fat. Empagliflozin and other SGLT-2 inhibitors are used to lower blood sugar in adults with T2DM.

Dr. Mithal and colleagues from Medanta-The Medicity Hospital hoped to determine if empagliflozin could reduce liver fat in T2DM patients with NAFLD; they presented their E-LIFT trial as a 

 at the ENDO 2018 annual meeting in Chicago, Illinois.

The E-LIFT trial is a single-center, prospective, open-label, randomized controlled trial looking at 50 patients with T2DM and NAFLD. Subjects were randomized to receive standard treatment for T2DM plus empagliflozin or standard treatment without empagliflozin. The primary outcome was liver fat change over 20 weeks.

Empagliflozin combined with standard treatment reduced the amount of liver fat more than standard treatment alone (4%; p<.0001).

At the end of 20 weeks MRI-derived proton density fat fraction was 11.3% vs 16.2% at baseline in the empagliflozin group (P<.0001) and 15.5% vs 16.4%, respectively, in the standard-treatment group (P=.057).

ALT, AST, and GGT were lowered in the empagliflozin group (–10.9 IU/L, P=0.005, –7.7 IU/L; P=.212 and –11 IU/L; P=.057 respectively). 

There were no significant differences between fasting plasma glucose and HbA1C between the empagliflozin and control groups at 20 weeks (p=0.850; HbA1C, p=0.880 respectively).

Adding empagliflozin to standard treatment for T2DM significantly reduced liver fat at 20 weeks compared to standard treatment alone.

No significant differences between groups were found with regards to HbA1c or fasting glucose levels.

“While our findings do not prove that empagliflozin will help treat NAFLD or prevent NASH, the initial results are promising and open up the possibility that empagliflozin may provide additional benefits for patients with diabetes,” Dr. Mithal stated. 

Kuchay MS, Krishan S, Mishra SK, Mithal A. 

Effect of empagliflozin on liver fat in patients with type 2 diabetes and nonalcoholic fatty liver disease: a randomized controlled trial (E-LIFT trial).

 Paper presented at The Endocrine Society Annual Meeting (ENDO 2018); March 2018; Chicago, IL.

Empagliflozin shown to significantly reduce liver fat in patients with T2DM, according to a new study. 