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1. DCRM 2.0: Multispecialty practice recommendations for the management of diabetes, cardiorenal, and metabolic diseases

Author

Handelsman, Yehuda, Anderson, John E., Bakris, George L., Ballantyne, Christie M., Bhatt, Deepak L., Bloomgarden, Zachary T., Bozkurt, Biykem, Budoff, Matthew J., Butler, Javed, Cherney, David Z.I., DeFronzo, Ralph A., Del Prato, Stefano, Eckel, Robert H., Filippatos, Gerasimos, Fonarow, Gregg C., Fonseca, Vivian A., Garvey, W. Timothy, Giorgino, Francesco, Grant, Peter J., Green, Jennifer B., Greene, Stephen J., Groop, Per-Henrik, Grunberger, George, Jastreboff, Ania M., Jellinger, Paul S., Khunti, Kamlesh, Klein, Samuel, Kosiborod, Mikhail N., Kushner, Pamela, Leiter, Lawrence A., Lepor, Norman E., Mantzoros, Christos S., Mathieu, Chantal, Mende, Christian W., Michos, Erin D., Morales, Javier, Plutzky, Jorge, Pratley, Richard E., Ray, Kausik K., Rossing, Peter, Sattar, Naveed, Schwarz, Peter E.H., Standl, Eberhard, Steg, P. Gabriel, Tokgözoğlu, Lale, Tuomilehto, Jaakko, Umpierrez, Guillermo E., Valensi, Paul, Weir, Matthew R., Wilding, John, and Wright, Eugene E., Jr.

Published
2024
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3. Second international consensus report on gaps and opportunities for the clinical translation of precision diabetes medicine

Author

Tobias, Deirdre K., Merino, Jordi, Ahmad, Abrar, Aiken, Catherine, Benham, Jamie L., Bodhini, Dhanasekaran, Clark, Amy L., Colclough, Kevin, Corcoy, Rosa, Cromer, Sara J., Duan, Daisy, Felton, Jamie L., Francis, Ellen C., Gillard, Pieter, Gingras, Véronique, Gaillard, Romy, Haider, Eram, Hughes, Alice, Ikle, Jennifer M., Jacobsen, Laura M., Kahkoska, Anna R., Kettunen, Jarno L. T., Kreienkamp, Raymond J., Lim, Lee-Ling, Männistö, Jonna M. E., Massey, Robert, Mclennan, Niamh-Maire, Miller, Rachel G., Morieri, Mario Luca, Most, Jasper, Naylor, Rochelle N., Ozkan, Bige, Patel, Kashyap Amratlal, Pilla, Scott J., Prystupa, Katsiaryna, Raghavan, Sridharan, Rooney, Mary R., Schön, Martin, Semnani-Azad, Zhila, Sevilla-Gonzalez, Magdalena, Svalastoga, Pernille, Takele, Wubet Worku, Tam, Claudia Ha-ting, Thuesen, Anne Cathrine B., Tosur, Mustafa, Wallace, Amelia S., Wang, Caroline C., Wong, Jessie J., Yamamoto, Jennifer M., Young, Katherine, Amouyal, Chloé, Andersen, Mette K., Bonham, Maxine P., Chen, Mingling, Cheng, Feifei, Chikowore, Tinashe, Chivers, Sian C., Clemmensen, Christoffer, Dabelea, Dana, Dawed, Adem Y., Deutsch, Aaron J., Dickens, Laura T., DiMeglio, Linda A., Dudenhöffer-Pfeifer, Monika, Evans-Molina, Carmella, Fernández-Balsells, María Mercè, Fitipaldi, Hugo, Fitzpatrick, Stephanie L., Gitelman, Stephen E., Goodarzi, Mark O., Grieger, Jessica A., Guasch-Ferré, Marta, Habibi, Nahal, Hansen, Torben, Huang, Chuiguo, Harris-Kawano, Arianna, Ismail, Heba M., Hoag, Benjamin, Johnson, Randi K., Jones, Angus G., Koivula, Robert W., Leong, Aaron, Leung, Gloria K. W., Libman, Ingrid M., Liu, Kai, Long, S. Alice, Lowe, Jr, William L., Morton, Robert W., Motala, Ayesha A., Onengut-Gumuscu, Suna, Pankow, James S., Pathirana, Maleesa, Pazmino, Sofia, Perez, Dianna, Petrie, John R., Powe, Camille E., Quinteros, Alejandra, Jain, Rashmi, Ray, Debashree, Ried-Larsen, Mathias, Saeed, Zeb, Santhakumar, Vanessa, Kanbour, Sarah, Sarkar, Sudipa, Monaco, Gabriela S. F., Scholtens, Denise M., Selvin, Elizabeth, Sheu, Wayne Huey-Herng, Speake, Cate, Stanislawski, Maggie A., Steenackers, Nele, Steck, Andrea K., Stefan, Norbert, Støy, Julie, Taylor, Rachael, Tye, Sok Cin, Ukke, Gebresilasea Gendisha, Urazbayeva, Marzhan, Van der Schueren, Bart, Vatier, Camille, Wentworth, John M., Hannah, Wesley, White, Sara L., Yu, Gechang, Zhang, Yingchai, Zhou, Shao J., Beltrand, Jacques, Polak, Michel, Aukrust, Ingvild, de Franco, Elisa, Flanagan, Sarah E., Maloney, Kristin A., McGovern, Andrew, Molnes, Janne, Nakabuye, Mariam, Njølstad, Pål Rasmus, Pomares-Millan, Hugo, Provenzano, Michele, Saint-Martin, Cécile, Zhang, Cuilin, Zhu, Yeyi, Auh, Sungyoung, de Souza, Russell, Fawcett, Andrea J., Gruber, Chandra, Mekonnen, Eskedar Getie, Mixter, Emily, Sherifali, Diana, Eckel, Robert H., Nolan, John J., Philipson, Louis H., Brown, Rebecca J., Billings, Liana K., Boyle, Kristen, Costacou, Tina, Dennis, John M., Florez, Jose C., Gloyn, Anna L., Gomez, Maria F., Gottlieb, Peter A., Greeley, Siri Atma W., Griffin, Kurt, Hattersley, Andrew T., Hirsch, Irl B., Hivert, Marie-France, Hood, Korey K., Josefson, Jami L., Kwak, Soo Heon, Laffel, Lori M., Lim, Siew S., Loos, Ruth J. F., Ma, Ronald C. W., Mathieu, Chantal, Mathioudakis, Nestoras, Meigs, James B., Misra, Shivani, Mohan, Viswanathan, Murphy, Rinki, Oram, Richard, Owen, Katharine R., Ozanne, Susan E., Pearson, Ewan R., Perng, Wei, Pollin, Toni I., Pop-Busui, Rodica, Pratley, Richard E., Redman, Leanne M., Redondo, Maria J., Reynolds, Rebecca M., Semple, Robert K., Sherr, Jennifer L., Sims, Emily K., Sweeting, Arianne, Tuomi, Tiinamaija, Udler, Miriam S., Vesco, Kimberly K., Vilsbøll, Tina, Wagner, Robert, Rich, Stephen S., and Franks, Paul W.

Published
2023
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6. Precision subclassification of type 2 diabetes: a systematic review

Author

Misra, Shivani, Wagner, Robert, Ozkan, Bige, Schön, Martin, Sevilla-Gonzalez, Magdalena, Prystupa, Katsiaryna, Wang, Caroline C., Kreienkamp, Raymond J., Cromer, Sara J., Rooney, Mary R., Duan, Daisy, Thuesen, Anne Cathrine Baun, Wallace, Amelia S., Leong, Aaron, Deutsch, Aaron J., Andersen, Mette K., Billings, Liana K., Eckel, Robert H., Sheu, Wayne Huey-Herng, Hansen, Torben, Stefan, Norbert, Goodarzi, Mark O., Ray, Debashree, Selvin, Elizabeth, Florez, Jose C., Meigs, James B., and Udler, Miriam S.

Published
2023
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7. DCRM Multispecialty Practice Recommendations for the management of diabetes, cardiorenal, and metabolic diseases.

Author

Handelsman, Yehuda, Anderson, John E, Bakris, George L, Ballantyne, Christie M, Beckman, Joshua A, Bhatt, Deepak L, Bloomgarden, Zachary T, Bozkurt, Biykem, Budoff, Matthew J, Butler, Javed, Dagogo-Jack, Samuel, de Boer, Ian H, DeFronzo, Ralph A, Eckel, Robert H, Einhorn, Daniel, Fonseca, Vivian A, Green, Jennifer B, Grunberger, George, Guerin, Chris, Inzucchi, Silvio E, Jellinger, Paul S, Kosiborod, Mikhail N, Kushner, Pamela, Lepor, Norman, Mende, Christian W, Michos, Erin D, Plutzky, Jorge, Taub, Pam R, Umpierrez, Guillermo E, Vaduganathan, Muthiah, and Weir, Matthew R

Subjects
Cardiovascular System, Humans, Cardiovascular Diseases, Diabetes Mellitus, Type 2, Hypoglycemic Agents, Renal Insufficiency, Chronic, Atherosclerotic cardiovascular disease, Chronic kidney disease, Clinical practice, Consensus recommendations, Heart failure, Type 2 diabetes, Kidney Disease, Diabetes, Clinical Trials and Supportive Activities, Clinical Research, Hepatitis, Heart Disease, Chronic Liver Disease and Cirrhosis, Liver Disease, Cardiovascular, Digestive Diseases, Prevention, Management of diseases and conditions, 7.1 Individual care needs, 7.3 Management and decision making, Metabolic and endocrine, Good Health and Well Being, Clinical Sciences, Endocrinology & Metabolism
Abstract

Type 2 diabetes (T2D), chronic kidney disease (CKD), atherosclerotic cardiovascular disease (ASCVD), and heart failure (HF)-along with their associated risk factors-have overlapping etiologies, and two or more of these conditions frequently occur in the same patient. Many recent cardiovascular outcome trials (CVOTs) have demonstrated the benefits of agents originally developed to control T2D, ASCVD, or CKD risk factors, and these agents have transcended their primary indications to confer benefits across a range of conditions. This evolution in CVOT evidence calls for practice recommendations that are not constrained by a single discipline to help clinicians manage patients with complex conditions involving diabetes, cardiorenal, and/or metabolic (DCRM) diseases. The ultimate goal for these recommendations is to be comprehensive yet succinct and easy to follow by the nonexpert-whether a specialist or a primary care clinician. To meet this need, we formed a volunteer task force comprising leading cardiologists, nephrologists, endocrinologists, and primary care physicians to develop the DCRM Practice Recommendations, a multispecialty consensus on the comprehensive management of the patient with complicated metabolic disease. The task force recommendations are based on strong evidence and incorporate practical guidance that is clinically relevant and simple to implement, with the aim of improving outcomes in patients with DCRM. The recommendations are presented as 18 separate graphics covering lifestyle therapy, patient self-management education, technology for DCRM management, prediabetes, cognitive dysfunction, vaccinations, clinical tests, lipids, hypertension, anticoagulation and antiplatelet therapy, antihyperglycemic therapy, hypoglycemia, nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH), ASCVD, HF, CKD, and comorbid HF and CKD, as well as a graphical summary of medications used for DCRM.

Published
2022

9. Clinical Care Pathway for the Risk Stratification and Management of Patients With Nonalcoholic Fatty Liver Disease

Author

Kanwal, Fasiha, Shubrook, Jay H, Adams, Leon A, Pfotenhauer, Kim, Wai-Sun Wong, Vincent, Wright, Eugene, Abdelmalek, Manal F, Harrison, Stephen A, Loomba, Rohit, Mantzoros, Christos S, Bugianesi, Elisabetta, Eckel, Robert H, Kaplan, Lee M, El-Serag, Hashem B, and Cusi, Kenneth

Subjects
Health Services, Clinical Research, Hepatitis, Liver Disease, Prevention, Digestive Diseases, Chronic Liver Disease and Cirrhosis, Oral and gastrointestinal, Good Health and Well Being, Clinical Decision-Making, Consensus, Critical Pathways, Decision Support Techniques, Evidence-Based Medicine, Gastroenterology, Humans, Non-alcoholic Fatty Liver Disease, Predictive Value of Tests, Risk Assessment, Risk Factors, Treatment Outcome, Nonalcoholic Fatty Liver Disease, NAFLD, Nonalcoholic Steatohepatitis, NASH, Clinical Care Pathway, Clinical Sciences, Neurosciences, Paediatrics and Reproductive Medicine, Gastroenterology & Hepatology
Abstract

Find AGA's NASH Clinical Care Pathway App for iOS and Android mobile devices at nash.gastro.org. Scan this QR code to be taken directly to the website.Nonalcoholic fatty liver disease (NAFLD) is becoming increasingly common, currently affecting approximately 37% of US adults. NAFLD is most often managed in primary care or endocrine clinics, where clinicians must determine which patients might benefit from secondary care to address hepatic manifestations, comorbid metabolic traits, and cardiovascular risks of the disease. Because NAFLD is largely asymptomatic, and because optimal timing of treatment depends on accurate staging of fibrosis risk, screening at the primary care level is critical, together with consistent, timely, evidence-based, widely accessible, and testable management processes. To achieve these goals, the American Gastroenterological Association assembled a multidisciplinary panel of experts to develop a Clinical Care Pathway providing explicit guidance on the screening, diagnosis, and treatment of NAFLD. This article describes the NAFLD Clinical Care Pathway they developed and provides a rationale supporting proposed steps to assist clinicians in diagnosing and managing NAFLD with clinically significant fibrosis (stage F2-F4) based on the best available evidence. This Pathway is intended to be applicable in any setting where care for patients with NAFLD is provided, including primary care, endocrine, obesity medicine, and gastroenterology practices.

Published
2021

11. Reply by Authors

Author

Crawford, E. David, Garnick, Marc B., Eckel, Robert H., Miner, Martin M., Freedland, Stephen J., Pachynski, Russell K., Wassersug, Richard J., Rosenberg, Matthew T., Walker, Lauren M., Fairman, Ciaran, Curley, Tracy, Crosby, Michael, Lin, Pao-Hwa, and Hafron, Jason M.

Published
2024
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14. Reduction in FSH Throughout the Menstrual Cycle After Omega-3 Fatty Acid Supplementation in Young Normal Weight but not Obese Women

Author

Bauer, Jessica L, Kuhn, Katherine, Bradford, Andrew P, Al-Safi, Zain A, Harris, Mary A, Eckel, Robert H, Robledo, Celeste Y, Malkhasyan, Anahit, Johnson, Joshua, Gee, Nancy R, and Polotsky, Alex J

Subjects
Reproductive Medicine, Biomedical and Clinical Sciences, Complementary and Integrative Health, Prevention, Contraception/Reproduction, Nutrition, Clinical Research, Estrogen, Obesity, Reproductive health and childbirth, Adult, Dietary Supplements, Docosahexaenoic Acids, Eicosapentaenoic Acid, Estrogens, Female, Follicle Stimulating Hormone, Humans, Luteinizing Hormone, Menstrual Cycle, Progestins, Young Adult, omega-3 polyunsaturated fatty acids, FSH, LH, obesity, fertility, Paediatrics and Reproductive Medicine, Obstetrics & Reproductive Medicine, Reproductive medicine, Midwifery
Abstract

Dietary fish oil restores ovarian function in subfertile rats, which is thought to be associated with decreased transcription of follicle-stimulating hormone (FSH) β-subunit. We have previously demonstrated a reduction in early follicular serum FSH levels in normal weight but not obese women after treatment with omega-3 polyunsaturated fatty acids (PUFA). Herein, we report the effect of supplementation with omega-3 PUFA on urinary reproductive hormones across the whole menstrual cycle. This interventional study included 17 eumenorrheic women, aged 24-41 years. One month of daily morning urine was collected before and after 1 month of omega-3 PUFA supplementation with 4 g of eicosapentaenoic acid and docosahexaenoic acid daily. Measurements included urinary FSH, luteinizing hormone (LH) and estrogen and progesterone metabolites, plasma fatty acid composition, and markers of endoplasmic reticulum stress. Compliance with dietary supplementation was verified by significantly reduced ratios of omega-6 to omega-3 PUFA for all subjects after treatment (P < .01). After 1 month of omega-3 PUFA supplementation, urinary FSH was significantly decreased in normal weight, but not obese women, in both follicular and luteal phases (-28.4% and -12.6%, respectively, both P = .04). No significant changes were seen in LH or sex steroids for either weight group. The selective and specific decrease in FSH suggests that omega-3 PUFA supplementation merits further investigation in normal weight women with decreased fertility and/or diminished ovarian reserve.

Published
2019

20. COVID-19 and metabolic disease: mechanisms and clinical management

Author

Steenblock, Charlotte, Schwarz, Peter E H, Ludwig, Barbara, Linkermann, Andreas, Zimmet, Paul, Kulebyakin, Konstantin, Tkachuk, Vsevolod A, Markov, Alexander G, Lehnert, Hendrik, de Angelis, Martin Hrabě, Rietzsch, Hannes, Rodionov, Roman N, Khunti, Kamlesh, Hopkins, David, Birkenfeld, Andreas L, Boehm, Bernhard, Holt, Richard I G, Skyler, Jay S, DeVries, J Hans, Renard, Eric, Eckel, Robert H, Alberti, K George M M, Geloneze, Bruno, Chan, Juliana C, Mbanya, Jean Claude, Onyegbutulem, Henry C, Ramachandran, Ambady, Basit, Abdul, Hassanein, Mohamed, Bewick, Gavin, Spinas, Giatgen A, Beuschlein, Felix, Landgraf, Rüdiger, Rubino, Francesco, Mingrone, Geltrude, and Bornstein, Stefan R

Published
2021
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26. Consequences of the COVID-19 pandemic for patients with metabolic diseases

Author

Bornstein, Stefan R., Rubino, Francesco, Ludwig, Barbara, Rietzsch, Hannes, Schwarz, Peter E. H., Rodionov, Roman N., Khunti, Kamlesh, Hopkins, David, Birkenfeld, Andreas L., Boehm, Bernhard, Amiel, Stephanie, Holt, Richard I. G., Skyler, Jay S., DeVries, J. Hans, Renard, Eric, Eckel, Robert H., Zimmet, Paul, Alberti, K. G., Geloneze, Bruno, Chan, Juliana C., Mbanya, Jean Claude, Onyegbutulem, Henry C., Ramachandran, Ambady, Basit, Abdul, Hassanein, Mohamed, Spinas, Giatgen A., Beuschlein, Felix, and Mingrone, Geltrude

Published
2021
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27. Bariatric and metabolic surgery during and after the COVID-19 pandemic: DSS recommendations for management of surgical candidates and postoperative patients and prioritisation of access to surgery

Author

Rubino, Francesco, Cohen, Ricardo V, Mingrone, Geltrude, le Roux, Carel W, Mechanick, Jeffrey I, Arterburn, David E, Vidal, Josep, Alberti, George, Amiel, Stephanie A, Batterham, Rachel L, Bornstein, Stefan, Chamseddine, Ghassan, Del Prato, Stefano, Dixon, John B, Eckel, Robert H, Hopkins, David, McGowan, Barbara M, Pan, An, Patel, Ameet, Pattou, François, Schauer, Philip R, Zimmet, Paul Z, and Cummings, David E

Published
2020
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29. Obesity development in neuron-specific lipoprotein lipase deficient mice is not responsive to increased dietary fat content or change in fat composition

Author

Wang, Hong, Taussig, Matthew D, DiPatrizio, Nicholas V, Bruce, Kimberley, Piomelli, Daniele, and Eckel, Robert H

Subjects
Biomedical and Clinical Sciences, Nutrition and Dietetics, Prevention, Neurosciences, Cardiovascular, Obesity, Nutrition, Heart Disease, Prevention of disease and conditions, and promotion of well-being, 3.3 Nutrition and chemoprevention, Metabolic and endocrine, Oral and gastrointestinal, Cancer, Stroke, Adiposity, Animals, Body Composition, Body Weight, Calorimetry, Indirect, Diet, High-Fat, Dietary Fats, Hypothalamus, Lipoprotein Lipase, Male, Mice, Mice, Knockout, Neurons, Lipoprotein lipase, n-3 PUFA, Dietary fat, CNS body weight regulation, Clinical Sciences, Endocrinology & Metabolism, Clinical sciences
Abstract

We have previously reported that mice with neuron-specific LPL deficiency (NEXLPL-/-) become obese by 16weeks of age on chow. Moreover, these mice had reduced uptake of triglyceride (TG)-rich lipoprotein-derived fatty acids and lower levels of n-3 long chain polyunsaturated fatty acids (n-3 PUFAs) in the hypothalamus. Here, we asked whether increased dietary fat content or altered dietary composition could modulate obesity development in NEXLPL-/- mice. Male NEXLPL-/- mice and littermate controls (WT) were randomly assigned one of three synthetic diets; a high carbohydrate diet (HC, 10% fat), a high-fat diet (HF, 45% fat), or a HC diet supplemented with n-3 PUFAs (HCn-3, 10% fat, Lovaza, GSK®). After 42weeks of HC feeding, body weight and fat mass were increased in the NEXLPL-/- mice compared to WT. WT mice fed a HF diet displayed typical diet-induced obesity, but weight gain was only marginal in HF-fed NEXLPL-/- mice, with no significant difference in body composition. Dietary n-3 PUFA supplementation did not prevent obesity in NEXLPL-/- mice, but was associated with differential modifications in hypothalamic gene expression and PUFA concentration compared to WT mice. Our findings suggest that neuronal LPL is involved in the regulation of body weight and composition in response to either the change in quantity (HF feeding) or quality (n-3 PUFA-enriched) of dietary fat. The precise role of LPL in lipid sensing in the brain requires further investigation.

Published
2016

30. Joint international consensus statement for ending stigma of obesity

Author

Rubino, Francesco, Puhl, Rebecca M., Cummings, David E., Eckel, Robert H., Ryan, Donna H., Mechanick, Jeffrey I., and Nadglowski, Joe

Subjects
Obesity -- Social aspects, Overweight persons -- Social aspects, Stigma (Social psychology) -- Control -- Social aspects, Biological sciences, Health
Abstract

People with obesity commonly face a pervasive, resilient form of social stigma. They are often subject to discrimination in the workplace as well as in educational and healthcare settings. Research indicates that weight stigma can cause physical and psychological harm, and that affected individuals are less likely to receive adequate care. For these reasons, weight stigma damages health, undermines human and social rights, and is unacceptable in modern societies. To inform healthcare professionals, policymakers, and the public about this issue, a multidisciplinary group of international experts, including representatives of scientific organizations, reviewed available evidence on the causes and harms of weight stigma and, using a modified Delphi process, developed a joint consensus statement with recommendations to eliminate weight bias. Academic institutions, professional organizations, media, public-health authorities, and governments should encourage education about weight stigma to facilitate a new public narrative about obesity, coherent with modern scientific knowledge., Author(s): Francesco Rubino [sup.1] [sup.2] , Rebecca M. Puhl [sup.3] , David E. Cummings [sup.4] [sup.5] , Robert H. Eckel [sup.6] [sup.7] , Donna H. Ryan [sup.8] , Jeffrey I. [...]

Published
2020
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34. Lipoprotein lipase is an important modulator of lipid uptake and storage in hypothalamic neurons

Author

Libby, Andrew E, Wang, Hong, Mittal, Richa, Sungelo, Mitchell, Potma, Eric, and Eckel, Robert H

Subjects
Biochemistry and Cell Biology, Biological Sciences, Nutrition, Neurosciences, Aetiology, 2.1 Biological and endogenous factors, Neurological, Metabolic and endocrine, Agouti-Related Protein, Animals, Apolipoproteins, Biological Transport, Cell Line, Transformed, Gene Expression, Genetic Vectors, Homeostasis, Humans, Hypothalamus, Lipid Droplets, Lipid Metabolism, Lipoprotein Lipase, Mice, Neurons, Retroviridae, Signal Transduction, Triglycerides, Lipoprotein lipase, AgRP, Lipid droplets, Medicinal and Biomolecular Chemistry, Medical Biochemistry and Metabolomics, Biochemistry & Molecular Biology, Biochemistry and cell biology, Medicinal and biomolecular chemistry
Abstract

LPL is the rate-limiting enzyme for uptake of TG-derived FFA in peripheral tissues, and the enzyme is expressed in the brain and CNS. We previously created a mouse which lacks neuronal LPL. This animal becomes obese on a standard chow, and we observed reduced lipid uptake in the hypothalamus at 3 months preceding obesity. In our present study, we replicated the animal phenotype in an immortalized mouse hypothalamic cell line (N41) to examine how LPL affects expression of AgRP as well as entry and storage of lipids into neurons. We show that LPL is able to modulate levels of the orexigenic peptide AgRP. LPL also exerts effects on lipid uptake into culture neurons, and that uptake of neutral lipid can be enhanced even by mutant LPL lacking catalytic activity. N41 cells also accumulate neutral lipid in droplets, and this is at least in part regulated by LPL. These data in addition to those published in mice with neuron-specific deletion of LPL suggest that neuronal LPL is an important regulator of lipid homeostasis in neurons and that alterations in LPL levels may have important effects on systemic metabolism and neuronal lipid biology.

Published
2015

35. Update on Prevention of Cardiovascular Disease in Adults With Type 2 Diabetes Mellitus in Light of Recent Evidence

Author

Fox, Caroline S, Golden, Sherita Hill, Anderson, Cheryl, Bray, George A, Burke, Lora E, de Boer, Ian H, Deedwania, Prakash, Eckel, Robert H, Ershow, Abby G, Fradkin, Judith, Inzucchi, Silvio E, Kosiborod, Mikhail, Nelson, Robert G, Patel, Mahesh J, Pignone, Michael, Quinn, Laurie, Schauer, Philip R, Selvin, Elizabeth, and Vafiadis, Dorothea K

Subjects
Clinical Research, Heart Disease, Nutrition, Cardiovascular, Diabetes, Prevention, Metabolic and endocrine, Good Health and Well Being, American Heart Association, Cardiovascular Diseases, Diabetes Mellitus, Type 2, Humans, Practice Guidelines as Topic, Primary Prevention, Randomized Controlled Trials as Topic, Risk Factors, United States, American Heart Association Diabetes Committee of the Council on Lifestyle and Cardiometabolic Health, Council on Clinical Cardiology, Council on Cardiovascular and Stroke Nursing, Council on Cardiovascular Surgery and Anesthesia, Council on Quality of Care and Outcomes Research, and the American Diabetes Association, AHA Scientific Statements, cardiovascular disease, diabetes, primary prevention, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Public Health and Health Services, Cardiovascular System & Hematology
Abstract

Cardiovascular disease risk factor control as primary prevention in patients with type 2 diabetes mellitus has changed substantially in the past few years. The purpose of this scientific statement is to review the current literature and key clinical trials pertaining to blood pressure and blood glucose control, cholesterol management, aspirin therapy, and lifestyle modification. We present a synthesis of the recent literature, new guidelines, and clinical targets, including screening for kidney and subclinical cardiovascular disease for the contemporary management of patients with type 2 diabetes mellitus.

Published
2015

36. Deficiency of Lipoprotein Lipase in Neurons Decreases AMPA Receptor Phosphorylation and Leads to Neurobehavioral Abnormalities in Mice

Author

Yu, Tian, Taussig, Matthew D, DiPatrizio, Nicholas V, Astarita, Giuseppe, Piomelli, Daniele, Bergman, Bryan C, Dell’Acqua, Mark L, Eckel, Robert H, and Wang, Hong

Subjects
Biological Psychology, Biomedical and Clinical Sciences, Psychology, Alzheimer's Disease, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Aging, Dementia, Behavioral and Social Science, Mental Health, Acquired Cognitive Impairment, Nutrition, Neurodegenerative, Neurosciences, Basic Behavioral and Social Science, Brain Disorders, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Aetiology, Underpinning research, Neurological, Amyloid beta-Peptides, Animals, Behavior, Animal, Cerebral Cortex, Cognition Disorders, Disease Models, Animal, Gene Expression, Genotype, Hippocampus, Learning, Lipid Metabolism, Lipoprotein Lipase, Memory, Metabolome, Metabolomics, Mice, Mice, Knockout, Neurodegenerative Diseases, Phosphorylation, Protein Subunits, Receptors, AMPA, General Science & Technology
Abstract

Alterations in lipid metabolism have been found in several neurodegenerative disorders, including Alzheimer's disease. Lipoprotein lipase (LPL) hydrolyzes triacylglycerides in lipoproteins and regulates lipid metabolism in multiple organs and tissues, including the central nervous system (CNS). Though many brain regions express LPL, the functions of this lipase in the CNS remain largely unknown. We developed mice with neuron-specific LPL deficiency that became obese on chow by 16 wks in homozygous mutant mice (NEXLPL-/-) and 10 mo in heterozygous mice (NEXLPL+/-). In the present study, we show that 21 mo NEXLPL+/- mice display substantial cognitive function decline including poorer learning and memory, and increased anxiety with no difference in general motor activities and exploratory behavior. These neurobehavioral abnormalities are associated with a reduction in the 2-amino-3-(3-hydroxy-5-methyl-isoxazol-4-yl) propanoic acid (AMPA) receptor subunit GluA1 and its phosphorylation, without any alterations in amyloid β accumulation. Importantly, a marked deficit in omega-3 and omega-6 polyunsaturated fatty acids (PUFA) in the hippocampus precedes the development of the neurobehavioral phenotype of NEXLPL+/- mice. And, a diet supplemented with n-3 PUFA can improve the learning and memory of NEXLPL+/- mice at both 10 mo and 21 mo of age. We interpret these findings to indicate that LPL regulates the availability of PUFA in the CNS and, this in turn, impacts the strength of synaptic plasticity in the brain of aging mice through the modification of AMPA receptor and its phosphorylation.

Published
2015

41. Residual vascular risk in diabetes – Will the SPPARM alpha concept hold the key?

Author

Fruchart, Jean-Charles, Santos, Raul D., Yamashita, Shizuya, Aikawa, Masanori, Libby, Peter, Plutzky, Jorge, Pradhan, Aruna, Ridker, Paul, Aguilar-Salinas, Carlos, Al Rasadi, Khalid, Amarenco, Pierre, Barter, Philip J., Ceska, Richard, Corsini, Alberto, Ruscica, Massimiliano, Després, Jean-Pierre, Duriez, Patrick, Eckel, Robert H., Ezhov, Marat V., Farnier, Michel, Ginsberg, Henry N., Hermans, Michel P., Ishibashi, Shun, Karpe, Fredrik, Kodama, Tatsuhiko, Koenig, Wolfgang, Krempf, Michel, Lim, Soo, Lorenzatti, Alberto J., McPherson, Ruth, Nuñez-Cortes, Jesus Millan, Nordestgaard, Børge G., Ogawa, Hisao, Packard, Chris J., Ponte-Negretti, Carlos I., Reiner, Željko, Sadikot, Shaukat, Shimano, Hitoshi, Sritara, Piyamitr, Stock, Jane K., Su, Ta-Chen, Susekov, Andrey V., Tartar, André, Taskinen, Marja-Riitta, Tenenbaum, Alexander, Tokgözoğlu, Lale S., Tomlinson, Brian, Tybjærg-Hansen, Anne, Valensi, Paul, Vrablík, Michal, Wahli, Walter, Watts, Gerald F., Yokote, Koutaro, and Zambon, Alberto

Published
2019
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42. Cardio‐renal‐metabolic disease in primary care setting.

Author

Ibrahim, Mahmoud, Ba‐Essa, Ebtesam M., Baker, Jason, Cahn, Avivit, Ceriello, Antonio, Cosentino, Francesco, Davies, Melanie J., Eckel, Robert H., Van Gaal, Luc, Gaede, Peter, Handelsman, Yehuda, Klein, Samuel, Leslie, Richard David, Pozzilli, Paolo, Del Prato, Stefano, Prattichizzo, Francesco, Schnell, Oliver, Seferovic, Petar M., Standl, Eberhard, and Thomas, Abraham

Subjects
CONTINUOUS glucose monitoring, PRIMARY care, TYPE 2 diabetes, HYPOGLYCEMIA, HEART diseases
Abstract

In the primary care setting providers have more tools available than ever before to impact positively obesity, diabetes, and their complications, such as renal and cardiac diseases. It is important to recognise what is available for treatment taking into account diabetes heterogeneity. For those who develop type 2 diabetes (T2DM), effective treatments are available that for the first time have shown a benefit in reducing mortality and macrovascular complications, in addition to the well‐established benefits of glucose control in reducing microvascular complications. Some of the newer medications for treating hyperglycaemia have also a positive impact in reducing heart failure (HF). Technological advances have also contributed to improving the quality of care in patients with diabetes. The use of technology, such as continuous glucose monitoring systems (CGM), has improved significantly glucose and glycated haemoglobin A1c (HbA1c) values, while limiting the frequency of hypoglycaemia. Other technological support derives from the use of predictive algorithms that need to be refined to help predict those subjects who are at great risk of developing the disease and/or its complications, or who may require care by other specialists. In this review we also provide recommendations for the optimal use of the new medications; sodium‐glucose co‐transporter‐2 inhibitors (SGLT2i) and Glucagon‐like peptide‐receptor agonists 1 (GLP1RA) in the primary care setting considering the relevance of these drugs for the management of T2DM also in its early stage. [ABSTRACT FROM AUTHOR]

Published
2024
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43. Reply by Authors

Author

Crawford, E. David, primary, Garnick, Marc B., additional, Eckel, Robert H., additional, Miner, Martin M., additional, Freedland, Stephen J., additional, Pachynski, Russell K., additional, Wassersug, Richard J., additional, Rosenberg, Matthew T., additional, Walker, Lauren M., additional, Fairman, Ciaran, additional, Curley, Tracy, additional, Crosby, Michael, additional, Lin, Pao-Hwa, additional, and Hafron, Jason M., additional

Published
2023
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47. Deficiency of Lipoprotein Lipase in Neurons Modifies the Regulation of Energy Balance and Leads to Obesity

Author

Wang, Hong, Astarita, Giuseppe, Taussig, Matthew D, Bharadwaj, Kalyani G, DiPatrizio, Nicholas V, Nave, Klaus-Armin, Piomelli, Daniele, Goldberg, Ira J, and Eckel, Robert H

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Nutrition, Neurosciences, Obesity, Metabolic and endocrine, Animals, Brain, Energy Intake, Energy Metabolism, Fatty Acids, Nonesterified, Female, Gene Expression, Hypothalamus, Lipoprotein Lipase, Lipoproteins, Male, Mice, Mice, Obese, Mice, Transgenic, Neurons, Medical Biochemistry and Metabolomics, Endocrinology & Metabolism, Biochemistry and cell biology, Medical biochemistry and metabolomics
Abstract

Free fatty acids (FFAs) suppress appetite when injected into the hypothalamus. To examine whether lipoprotein lipase (LPL), a serine hydrolase that releases FFAs from circulating triglyceride (TG)-rich lipoproteins, might contribute to FFA-mediated signaling in the brain, we created neuron-specific LPL-deficient mice. Homozygous mutant (NEXLPL-/-) mice were hyperphagic and became obese by 16 weeks of age. These traits were accompanied by elevations in the hypothalamic orexigenic neuropeptides, AgRP and NPY, and were followed by reductions in metabolic rate. The uptake of TG-rich lipoprotein fatty acids was reduced in the hypothalamus of 3-month-old NEXLPL-/- mice. Moreover, deficiencies in essential fatty acids in the hypothalamus were evident by 3 months, with major deficiencies of long-chain n-3 fatty acids by 12 months. These results indicate that TG-rich lipoproteins are sensed in the brain by an LPL-dependent mechanism and provide lipid signals for the central regulation of body weight and energy balance.

Published
2011

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