New obesity therapies were not boradly represented at this year's EASD – in fact, Novo Nordisk held the only presence within obesity pharmacotherapies, with a strong showing of SCALE data for Saxenda (liraglutide 3.0 mg for obesity). Dr. Arya Sharma (University of Alberta, Edmonton, Canada) first opened Novo Nordisk’s corporate symposium on Monday with a motivating presentation as to how we should frame obesity as a key driver of the global diabetes epidemic. From there, the rest of the focus centered around Saxenda, which recently received a vote in favor of approval from the FDA Advisory Committee. We saw new follow-up data that demonstrated the need for long-term treatment of Saxenda. For example, in a follow-up study as part of the SCALE Prediabetes trial, Dr. Xavier Pi-Sunyer (Columbia University, New York, NY) showed that patients that discontinued Saxenda therapy regained weight and saw a rebound in prediabetes incidence compared to those who stayed on the treatment. Similarly, Dr. Ralph DeFronzo (University of Texas Health Science Center, San Antonio, TX) investigated the effect of ceasing Saxenda treatment in an off-treatment follow-up period after the original SCALE Diabetes trial and also found a rapid reversal of the benefits seen with treatment. We heard very little on Vivus’ Qsymia (phentermine/topiramate ER), Arena/Eisai’s Belviq (lorcaserin), and Orexigen’s recently approved Contrave (naltrexone/bupropion). Along with the recent news of Novo Nordisk’s plans to establish a new obesity research unit, the company’s obesity presence at EASD excites us about the way that the company might be able to blur the lines between obesity and diabetes therapy.
Below we outline the key talks in obesity, followed by a table of contents and our detailed reporting. Titles highlighted in blue are new additions that were not mentioned in our daily updates from Vienna, and those highlighted in yellow represent what we felt were the most notable talks of the meeting.
- Executive Highlights
- Oral Presentations: GLP-1 Analogues – Clinical Efficacy
- Effect of Liraglutide 3.0 mg Cessation on Efficacy and Safety Tolerability After 56 Weeks’ Treatment in Obese/Overweight Adults with Type 2 Diabetes: SCALE Diabetes
- Liraglutide 3.0 mg Reduces the Prevalence of Prediabetes and Delays Onset of Type 2 Diabetes in Overweight/Obese Adults: The SCALE Obesity and Prediabetes Trial
- Liraglutide 3.0 mg for Weight Management in Obese/Overweight Adults with Type 2 Diabetes: SCALE Diabetes 56-Week Randomized, Double-Blind, Placebo-Controlled Trial
- Oral Presentations: Weight Regulation and Obesity
- Oral Presentations: Physiological Adaptation to Bariatric Surgery
- Beta Cell Function Improvements in Subjects with Type 2 Diabetes 1 Year After Biliopancreatic Diversion
- Mechanisms of Post-Prandial Hypoglycemia After Roux-en-Y Gastric Bypass (RYGB) and Sleeve Gastrectomy (LSG)
- Restoration of Beta Cell Function in Severely Obese Type 2 Diabetic Patients AFter Gastric Bypass Surgery Is Accompanied by Improved Insulin Processing
- Symposium: Face Diabetes – Therapeutic Strategies (Sponsored by Österreichische Diabetes Gesellschaft)
- Corporate Symposium: Building a Brighter Future – Addressing Challenges in Patient Care (Sponsored by Novo Nordisk)
- Oral Presentations: GLP-1 Analogues – Clinical Efficacy
Oral Presentations: GLP-1 Analogues – Clinical Efficacy
Ralph DeFronzo, MD (UT Health Science Center, San Antonio, TX)
Dr. Ralph DeFronzo presented results from a 12-week off-treatment follow-up period after the SCALE Diabetes trial that investigated the effect of ceasing liraglutide 3.0 mg treatment on safety and efficacy parameters. Those who completed 56 weeks’ treatment of the original trial (n=628) entered the off-treatment follow-up. The results demonstrated that following the cessation of liraglutide 3.0 mg treatment, the drug’s beneficial effects on weight, fasting plasma glucose, and systolic blood pressure were all rapidly reversed. Specifically, at 56 weeks (the beginning of the follow-up), the liraglutide 3.0 mg group had a mean weight loss of 6.7% from a baseline of 106 kg (234 lbs.); at 68 weeks, the group gained 2% in weight for a mean weight loss from baseline of 4.7%; however, this was still greater than the 2.5% weight loss from baseline in the placebo group. FPG reverted toward placebo levels within two weeks of treatment cessation; at 68 weeks, change in FPG from a baseline of 8.8 mmol/L was only -0.21 mmol/L for liraglutide 3.0 mg (compared to -1.9 mmol/L at week 56). Notably, the increases in pulse rate and lipase activity were also reversed once treatment was removed – at week 68, liraglutide 3.0 mg had a pulse rate reduction of 1.3 beats per minute and lipase activity was similar in all treatment groups. No safety signals were identified following treatment cessation. To see the results of the original SCALE Diabetes trial, see our coverage from this year’s ADA.
Questions and Answers
Q: Can you speculate on how important the nausea effect is in kicking off the weight reduction through possibly either meal size or frequency?
A: In the people who experienced nausea, a small percentage did have some transient vomiting. Clearly, this played some role in these patients. But when you look at the entire database, there was no relationship between the incidence of nausea and the weight loss. So I think in large part, this is essentially a mediated effect. I think the studies presented earlier provided some insight on what’s going on because there clearly are effects of exenatide that are global, not only in the hypothalamus – but I think we’re starting to recognize that throughout the food reward system, there are major effects of the GLP-1 receptor agonist.
Q: As I could see from the difference between cardiovascular effects of the two doses, I could see that the lower dose has better effects on blood pressure and pulse. Do you have any explanation for this?
A: Actually, there was no difference in change of blood pressure between the two doses. Interestingly, there was actually no dose response for 1.8 mg and 3.0 mg – they were virtually identical. The lines wiggled and crossed each other. There was a small difference in pulse rate. But, I would not say that there was a significant dose response between the two doses. Of course, the blood pressure decrease is something that would be considered very beneficial. The rise in pulse is very controversial – while we tend to think this is bad, we need to realize that all of this data relating pulse to adverse cardiovascular events comes from epidemiological studies and not from prospective studies. So the significance of this rise in pulse remains to be seen. We do have a long-term cardiovascular study ongoing, which will hopefully put this question to rest.
Xavier Pi-Sunyer, MD, PhD (Columbia University, New York, NY)
The renowned Dr. Xavier Pi-Sunyer presented data from the phase 3 SCALE Obesity and Prediabetes trial, which we covered previously at this year’s ICE/ENDO. The trial showed that Novo Nordisk’s liraglutide 3.0 mg (Saxenda) reduced the risk of developing type 2 diabetes in overweight and obese adults with normoglycemia by ~65%. In this session, Dr. Pi-Sunyer notably presented new follow-up results from between 56 and 68 weeks, in which participants were re-randomized from the liraglutide 3.0 mg group to either stay on treatment or revert to placebo. Those in the new placebo group regained more weight than those who remained on the drug (2.9% vs. 0.7%); the prevalence of prediabetes rose to a greater extent in the new placebo group (from 8.0% to 22.4%) than in the liraglutide 3.0 mg group (from 9.1% to 8.6%). Dr. Pi-Sunyer noted that no participants in either group developed type 2 diabetes during this re-randomized period. Big-picture, these results demonstrate that it is necessary to stay on liraglutide 3.0 mg for its sizeable metabolic benefits to persist. The need for chronic usage perhaps raises the stakes for the drug’s long-term safety assessment, a factor that came up during the FDA Advisory Committee meeting on liraglutide 3.0 mg for obesity earlier this fall.
Questions and Answers
Q: What was pancreatitis like in the placebo group?
A: There was slightly more pancreatitis in the drug group compared to the placebo group. All of the pancreatitis reversed very quickly with the withdrawal of the drug.
Q: Losing weight decreases insulin secretion. How do insulin levels behave in this case? Are there any episodes of hypoglycemia?
A: Hypoglycemia was tracked through OGTT and there was some hypoglycemia, but hypoglycemia was not severe at all in these patients so they maintained their euglycemia quite well. As you know, this is in the nature of liraglutide. When the glucose gets below a certain point, the activity disappears with regard to insulin secretory responses. Insulin levels with liraglutide do go up with GLP-1 therapy and you would expect that.
Q: Should we actually change clinical practice for this group of patients to use a drug that we need to continue to use to see effects?
A: I think that’s a question for every practitioner. As you know, the 3.0 mg dose is not approved yet. It is currently being looked at by both the FDA and EMA. If and when approved, that is up to the practitioner and it will depend a lot on the nature of the patient being treated – the degree of obesity, insulin resistance, compliance, and willingness to do lifestyle change. There’s no point in using the drug if the patient does no lifestyle change at all. This trial that I showed you connected both the lifestyle intervention with the drug and I think that’s how it should be used over time.
Melanie Davies, MD (University of Leicester, UK)
Dr. Melanie Davies presented phase 3a results from the 56-week SCALE Diabetes trial, which assessed the efficacy of Novo Nordisk’s liraglutide 3.0 mg for weight management in 846 overweight or obese adults with type 2 diabetes – we previously covered this data at this year’s ADA. Placebo-adjusted weight loss was on the modest side, at 3.9%; this was likely due to the patient population selected, as placebo-adjusted weight loss was greater than 5% for the entire SCALE program. The 0.9% placebo-adjusted A1c reduction (from a baseline of 8%) was impressive, though not unexpected. Dr. Davies also presented data on heart rate, demonstrating that liraglutide 3.0 mg had an increase of 3.4 beats/min, from a mean baseline pulse rate of 74.2 beats/min.
Questions and Answers
Q: When would you envision people would want to use the 3.0 mg dose? Have you measured quality of life?
A: We did measure patient outcome measures and treatment satisfaction was greater in the 3.0 mg dose. There appears to be very significant benefits at the 1.8 mg dose, but greater benefits with the 3.0 mg. There were a greater number of patients reaching their A1c targets in 3.0 mg and if you look at other cardiovascular data, while both doses gave benefits, triglycerides and lipids saw greater benefits with the 3.0 mg dose.
Q: Do we need to increase the liraglutide dose from 1.8 mg to 3.0 mg for all of our patients taking this drug?
A: You raise an important point. In terms of safety and tolerability between 1.8 and 3.0 mg, apart from GI side effects, we don’t see increases in heart rate, etc. We don’t think that this study showed us how to use 1.8 mg or when to switch – we just know that going 1.8 mg to 3.0 mg gets more people to target and has more benefits. In clinical practice, it may be difficult to pick out who needs 3.0 mg, but data shows that 3.0 mg has a greater benefit overall.
Q: This question is related to metformin and Victoza – there are clinical observations that metformin may be related to nausea and other GI side effects. Have you done a subgroup analysis of those on metformin or adjusted the metformin dosing?
A: Around 57% of the patients had a background of metformin. We did not really attempt to reduce their dose – this was maintained stable throughout the study. There was some reduction in the dose of sulfonylureas. We didn’t look at a subgroup analysis. There are probably better data sets out there looking at metformin and liraglutide.
Q: Did you see any increases in atrial fibrillation rate? If so, was there a difference between the doses?
A: We saw one case of atrial fibrillation, which we saw in the liraglutide 3.0 mg group. Since this was only one case, we didn’t identify a signal of arrhythmia or atrial fibrillation. But there was the increase in heart rate.
Oral Presentations: Weight Regulation and Obesity
Endogenous GLP-1 Alters Brain Activations in Response to Visual Food-Cues in Reward and Satiety Circuits in Humans
Jennifer Sylvia ten Kulve, MD (University of Amsterdam, Netherlands)
Results from an fMRI analysis presented by Dr. Jennifer Sylvia ten Kulve support the hypothesis that endogenous GLP-1 has an effect on the central nervous system’s satiety circuitry and contributes to the regulation of feeding. The study investigated the effect of administering exendin 9-39, a GLP-1 receptor antagonist, or saline on reward and satiety circuit activation in response to visual food cues in 20 obese individuals with type 2 diabetes (Average BMI: 32 kg/m2; treated with metformin and sulfonylureas only) against 20 normoglycemic and lean individuals (Average BMI: 22.5 kg/m2). Researchers administered drug (or placebo) 60 minutes prior to the visual-stimulation paradigm, then provided subjects with a standardized liquid meal (450 calories) and repeated the assessment. Results indicated that: (i) in the placebo state, reward circuitry activation is increased in the obese group relative to the lean group in response to visual food cues; (ii) following a meal, there is a reduction in CNS activity in response to food pictures in both lean and obese patients; and (iii) GLP-1 receptor blockade alters the effect of a meal on brain activity in response to food pictures and increases patients perceived hunger.
- The study enrolled 20 obese individual with type 2 diabetes (Average BMI: 32 kg/m2; Average A1c: ~7.3%) and 20 normoglycemic and lean individuals (Average BMI: 22.5 kg/m2; Average A1c: ~5.6%). The average age of the lean cohort was 56 years and that of the obese cohort was 60 years. The male/female spilt was 10/10 and 11/9 in the lean and obese groups, respectively. Duration of diabetes was not reported.
- Study Design: Researchers administered drug (or placebo) 60 minutes prior to the visual-stimulation paradigm. Subjects were then provided with a standardized liquid meal (450 calories) and the fMRI-visual stimulation paradigm was again administered. Thirty minutes separated the two visual-stimulation protocols.
- fMRI Design and Measurement: The visual stimulation paradigm consisted of a block design that rotated between high calorie (e.g., French fries, cake), low calorie (e.g., fruit, vegetables), and neutral (e.g., trees) images. The CNS response was determined by taking the difference in the response to food and neutral pictures. Responses to high calorie vs. low calorie images were not presented.
- Even in the absence of GLP-1 agonism, there were differences in lean and obese individuals’ responses to visual food cues. The obese group showed increased activation in the right orbitofrontal cortex (p=0.004), amygdala (p-value unknown), and right insula (p=0.019) in response to food pictures relative to the lean cohort. Dr. Kulve emphasized that these results are not novel; rather, they confirm prior findings established by her group.
- Intake of a liquid meal reduces reward and satiety circuit activation in response to visual food cues. In lean individuals, fMRI data indicated a significant decrease of activation in the right insula (p=0.024) in the post-prandial state relative to the fasting state. Results indicated a similar reduction in activity in the right (p=0.03) and left (trending toward significance, p=0.063) insula in obese individuals. Dr. Kulve did not discuss the significance of the reduced activity seen in both hemispheres in obese individuals; we find the result intriguing given that obese individuals typically show hyperactivation of the CNS.
- In obese individuals, blockade of GLP-1 receptors prevented the reduction in CNS activation following a meal. Notably, data from fMRI indicate that the resulting signal was significantly greater in patients administered with the drug as opposed to placebo in both the right (p=0.022) and left (p=0.028) insula. Results in lean individuals were not reported.
- Blockade of GLP-1 receptors also mitigated the postprandial decrease in hunger scores seen in placebo. Dr. Kulve did not describe the features of the hunger score or the methodology employed to collect this data; we assume the findings reflect a survey given to participants before the second visual stimulation paradigm. Results indicated that lean individuals administered placebo experienced a non-significant decrease in perceived hunger relative to those administered the GLP-1 antagonist. However, obese individuals administered placebo experienced a significant (p-value unknown) decrease in perceived hunger relative to those administered the GLP-1 antagonist. Notably, the findings suggests that GLP-1 receptor activation has an appetite-suppressing effect and highlight one pathway by which this drug class may constitute its effect on the CNS.
Questions and Answers
Q: Hyperglycemia from obesity. In your study, can we distinguish the effect of hyperglycemia from the effect of obesity? We know insulin resistance in the brain affects both of these areas? How much did high glucose affect this?
A: One of my colleagues, in a separate study, has examined three groups with obesity and type 2 diabetes and three groups with obesity alone. The findings are comparable in some areas, but diabetes is an additional contributing factor. I wouldn’t say that the effect of type 2 diabetes and obesity have the same effect as obesity alone. Slightly higher blood glucose levels could affect the CNS system. You should see them as different groups.
Q: How many food stimuli did you have? Did you compare whether or not the response was different between low calorie and high calorie foods?
A: We combined low and high pictures together in our analysis. The experiment took ten minutes with seven minutes for food pictures, so there were over 100 pictures of food during the session. We briefly dissected how patients responded to low high calorie foods. We could speculate that high caloric food pictures offer more of a hedonic reward that is related to feeding. We find more activation of some areas of the brain in response to high calorie foods. So, there does seem to be a different in response to high and low calorie pictures.
Q: Do you have any data on whether transport of GLP-1 agonists into the brain is affected by obesity?
A: I don’t have the data. I think if you take a measurement of cerebrospinal fluid that could help you determine that though.
Oral Presentations: Physiological Adaptation to Bariatric Surgery
Marcelo Lima, MD (University of Padova, Padova, Italy)
Dr. Marcelo Lima presented study results showing that biliopancreatic diversion (BPD) in obese patients with type 2 diabetes led to positive physiological adaptations with regards to beta cell function. For background, BPD is one of the most effective forms of bariatric surgery in terms of resolving dysglycemia, but is also one of the more severe and risky, involving severe malabsorption. This study confirmed BPD’s efficacy on glucose by showing that BPD increased insulin sensitivity to the same levels or even higher than the levels in patients with normal glucose tolerance. We have heard that BPD is on the rise in popularity, perhaps because of this marked efficacy in improving insulin resistance to near-healthy levels. The mechanism of action is likely dependent on increased incretin secretion, following more direct delivery of food to the distal small intestine.
- The study examined beta-cell function parameters and insulin sensitivity via a hyperglycemic clamp test and OGTT test. All participants were women of at least 20 years of age, and the study looked at three groups: one group (n=19) was composed of lean participants (BMI of 23 kg/m2) with normal glucose tolerance, another group (n=18) consisted of obese participants (BMI of 35 kg/m2) with normal glucose tolerance, and the third group (n=31) consisted of obese patients (BMI of 36 kg/m2) with type 2 diabetes who had undergone BPD. This third group was assessed at baseline and then 12 months post BPD. The results showed that after BPD, obese patients had increased insulin sensitivity up to the same levels or higher as the lean NGT group.
Questions and Answers
Q: The improvements in beta-cell function in response to the hyperglycemic clamp would suggest that improvements are not just due to bypassing gut hormones – so what’s the explanation? Is it calorie restriction or something else?
A: Nobody knows the answer but we have a few hypotheses. Calorie restriction seems to have a role, especially at the very beginning after bariatric surgery. It’s possible that the mid cells get some recovery over time in response to continuous stimuli from GLP-1 and other incretins. That would make them more responsive to glucose, even when intravenously infused. Lipotoxicity is relieved after surgery. Beta-cell function is also much potentiated by insulin sensitivity itself.
Q: Did you have the opportunity to use multiple linear regressions to see what variations in improvement in A1c could be accounted for by improvement in insulin sensitivity and secretion?
A: We did not have this opportunity, but in fact, we have other patients that have been studied so we have now a much greater group of patients that could be evaluated by this and next month. But we don’t have it right now.
Q: You had mentioned many aspects of beta-cell function. But what you’ve shown is global improvement. Could you speculate which of those aspects would be more important for improvement or are they all equally?
A: Biliopancreatic diversion has a very special effect in insulin sensitivity. It seems to have greater impact than other techniques, at least in the first months after surgery. Insulin sensitivity seems to be the most effective in biliopancreatic diversion.
Monica Nannipieri, MD, PhD (University of Pisa, Pisa, Italy)
Dr. Monica Nannipieri presented study results showing that lower plasma glucose concentrations and a lower insulin clearance before surgery are associated with higher risk of reactive hypoglycemia after roux-en-Y gastric bypass (RYGB) and sleeve gastrectomy (LSG). This form of hypoglycemia, which can sometimes be linked with gastric dumping syndrome, is severe and can even require a pancreatectomy. The study looked at obese non-diabetic participants treated with RYGB (n=31) or LSG (n=39). Each participant received a three-hour, 75 g oral glucose tolerance test (OGTT) both before surgery and 24 to 30 months after surgery. From the OGTT results, insulin secretion, beta-cell function, beta glucose sensitivity, and insulin sensitivity were determined through mathematical modeling. The findings showed that participants who experienced hypoglycemia after surgery had lower plasma glucose concentrations and insulin clearance prior to surgery compared to those who did not experience hypoglycemia. Insulin secretion levels, however, were relatively similar between the groups. Dr. Nannipieri concluded that mechanistically, inherently higher insulin output with a reduced insulin clearance and increased beta-cell glucose response account for postprandial hypoglycemia in surgically weight-reduced patients.
Questions and Answers
Q: Have you come up with an explanation for increased beta-cell sensitivity? Have you measured GLP-1 and DPP-4?
A: We measured GLP-1 but didn’t find any differences between the hypo and non-hypo patients. We’re now measuring GIP.
Comment: There is a paper out now that suggests that GLP-1 may be responsible.
A: Another recent paper described that those with hypoglycemia were treated with GLP-1 analogs and they recovered symptoms of hypoglycemia. So I think further studies will need to be done to understand this.
Q: That’s interesting that there is that difference between glucose clearance. Do you know the mechanism for this?
A: At the moment, we have no findings so we don’t know. It’s easy to understand that reduced glucose clearance makes hypoglycemia, but we don’t know why.
Eva Svehlikova, MD (Medical University of Graz, Graz, Austria)
Dr. Eva Svehlikova presented clinical trial results demonstrating improved insulin processing at the level of the beta cell, in addition to increased insulin sensitivity, following bariatric surgery in morbidly obese patients with type 2 diabetes. While diabetes remission after gastric bypass surgery has been extensively studied, the underlying mechanism is still poorly understood, and this study aimed to elucidate whether improved beta cell function contributes significantly to the observed improvements in glucose control. The study enrolled 55 severely obese patients (BMI = 43-44 kg/m2), 34 of whom had type 2 diabetes (A1c = 7.5%) and 21 of whom did not (A1c = 5.5%). Participants underwent an oral glucose tolerance test (OGTT), an intravenous glucose tolerance test (IVGTT), and a hyperinsulinemic-euglycemic clamp at three points: before, eight to 21 days after, and one year after bariatric surgery. Consistent with results from previous trials, both groups saw improvements in glucose control and insulin secretion following surgery, though there were still significant differences between patients with and without diabetes. There was a substantial increase in peripheral insulin sensitivity immediately after surgery and a further increase by the end of one year; in this measure, the type 2 diabetes group reached the baseline levels of the group without diabetes. Notably, the proinsulin/C-peptide ratio (an indicator of dysregulation in insulin processing by the beta cells) decreased rapidly after surgery and continued to decline for one year in the type 2 diabetes patients (patients without diabetes also saw a modest initial decrease from a lower baseline). This suggests that an improvement in beta cell function is at least one key component of the mechanism behind improved glucose control following bariatric surgery in obese patients with type 2 diabetes.
Questions and Answers
Q: I was surprised too see an improvement in peripheral insulin sensitivity. What dose of insulin did you use, and did you use tracers to assess hepatic glucose production?
A: I’ve read your paper on this subject. We had a higher dose of insulin than your study because of the setting; we had twice the dose during the study period. It’s true that the dose was not physiological, which may have influenced the results. And no, we did not use tracers.
Q: You showed a rapid restoration of the proinsulin/C-peptide ratio, which continued to improve. Why was there a further reduction in proinsulin after one year?
A: We can only speculate, but a further decrease in glucose toxicity associated with weight loss may have been a factor that supported beta cell function, so we continued to see a reduction in the ratio.
Q: Was there cross-reactivity with proinsulin?
A: I don’t have exact data on that.
Symposium: Face Diabetes – Therapeutic Strategies (Sponsored by Österreichische Diabetes Gesellschaft)
Bariatric Surgery – A Solution for Type 2 Diabetes Treatment?
Bernhard Ludvik, MD (Medical University of Vienna, Vienna, Austria)
Dr. Bernhard Ludvik advocated for the use of bariatric surgery as a treatment for type 2 diabetes, discussing its safety and efficacy, cost-effectiveness, as well as the mechanisms behind the positive impact on diabetes remission. With regards to efficacy, Dr. Ludvik cited data (Mingrone et al., NEJM 2012) showing that gastric bypass and biliopancreatic diversion achieved diabetes remission in 75% and 95% of patients, respectively (vs. no remission with medical therapy alone). He also noted that there were low rates of complications and few adverse events. In addition, he highlighted that having type 2 diabetes does not influence the long-term outcomes, as patients both with and without type 2 diabetes experienced comparable weight loss (-32% in T2DM vs. -28% in controls). Strengthening his case, Dr. Ludvik presented a short-term study (Ghiassi et al., Surgery for Obesity and Related Diseases, 2012) that reported an annual cost reduction of 69% for diabetes medications after gastric bypass surgery. Exploring the mechanisms behind bariatric surgery’s diabetes remission, Dr. Ludvik explained the effects of different procedures on beta-cell glucose sensitivity and GLP-1 secretion, suggesting that DPP-4 inhibitors and GLP-1 agonists would be unlikely candidates for therapy post-operation (we more frequently hear the opposite). He added that sulfonylureas may aggravate the postprandial hypoglycemia already present following surgery and that metformin, pioglitazone, SGLT-2 inhibitors, and insulin would instead make for appropriate therapeutic options.
Questions and Answers
Q: What do you think the role of EndoBarrier will be?
A: I honestly have no idea because it’s quite a recent development. And the data is not long enough. We don’t know about the long-term consequences. But I’m quite curious about this method – it’s a nice approach and it’s quite non-invasive.
Corporate Symposium: Building a Brighter Future – Addressing Challenges in Patient Care (Sponsored by Novo Nordisk)
The Impact of Weight on Metabolic Health: Building and Advancing Current Knowledge
Arya Sharma, MD, PhD (University of Alberta, Edmonton, Canada)
Dr. Arya Sharma opened Novo Nordisk’s massive daylong corporate symposium with a strong emphasis that obesity is a key driver of the global diabetes epidemic. In explaining this, he presented the skyrocketing rates of obesity throughout the world and how BMI correlates positively with insulin resistance. Moving beyond obesity’s connection with diabetes, Dr. Sharma also highlighted its association with cardiovascular risk, noting how the prevalence of hypertension increases with increasing BMI. He continued by acknowledging that obesity also brings about higher rates of obstructive sleep apnea (which he pointed out contributes to cardiovascular risk as well) and various types of cancer. Further supporting the gravity of obesity, he called attention to the reduced life expectancy and health-related quality of life of those with obesity. Concluding, Dr. Sharma emphasized that it is important to frame obesity in the context of the global diabetes epidemic, as a treatment for obesity can help treat all of these other conditions. Novo Nordisk’s decision to begin its symposium on the topic of obesity was rooted in the importance of the obesity epidemic in causing the rise in diabetes incidence, but it may also have been influenced by the company’s exciting recent decision to build a greater presence in obesity.
-- by Melissa An, Adam Brown, Varun Iyengar, Emily Regier, Manu Venkat, and Kelly Close
-- The authors thank Eric Chang, Hannah Deming, Jessica Dong, Nina Ran, and Melissa Tjota for additional help on conference writing and editing