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Article ; Online: Unraveling the actions of AMP-activated protein kinase in metabolic diseases: Systemic to molecular insights.

Weikel, Karen A / Ruderman, Neil B / Cacicedo, José M

2016 Volume 65, Issue 5, Page(s) 634–645

Abstract: AMP-activated protein kinase (AMPK) plays a critical role both in sensing and regulating cellular energy state. In experimental animals, its activation has been shown to reduce the risk of obesity and diabetes-related co-morbidities such as insulin ... ...

Abstract	AMP-activated protein kinase (AMPK) plays a critical role both in sensing and regulating cellular energy state. In experimental animals, its activation has been shown to reduce the risk of obesity and diabetes-related co-morbidities such as insulin resistance, the metabolic syndrome and atherosclerotic cardiovascular disease. However, in humans, AMPK activation alone often does not completely resolve these conditions. Thus, an improved understanding of AMPK action and regulation in metabolic and other diseases is needed. Herein, we provide a brief description of the enzymatic regulation of AMPK and review its role in maintaining energy homeostasis. We then discuss tissue-specific actions of AMPK that become distorted during such conditions as obesity, type 2 diabetes and certain cancers. Finally, we explore recent findings regarding the interactions of AMPK with mammalian target of rapamycin complex 1 and the lysosome and discuss how changes in these relationships during overnutrition may lead to AMPK dysfunction. A more thorough understanding of AMPK's molecular interactions during diseases of overnutrition may provide key insights for the development of AMPK-based combinatorial treatments for metabolic disease.
MeSH term(s)	AMP-Activated Protein Kinases/chemistry ; AMP-Activated Protein Kinases/metabolism ; Animals ; Energy Intake ; Energy Metabolism ; Glucose Metabolism Disorders/enzymology ; Glucose Metabolism Disorders/metabolism ; Humans ; Insulin Resistance ; Lysosomes/enzymology ; Lysosomes/metabolism ; Mechanistic Target of Rapamycin Complex 1 ; Models, Biological ; Multiprotein Complexes/metabolism ; Neoplasm Proteins/chemistry ; Neoplasm Proteins/metabolism ; Neoplasms/enzymology ; Neoplasms/metabolism ; Obesity/enzymology ; Obesity/metabolism ; Organ Specificity ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	Multiprotein Complexes ; Neoplasm Proteins ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2016-01-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	80230-x
ISSN	1532-8600 ; 0026-0495
ISSN (online)	1532-8600
ISSN	0026-0495
DOI	10.1016/j.metabol.2016.01.005
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Article ; Online: AMP-activated Protein Kinase (AMPK): Does This Master Regulator of Cellular Energy State Distinguish Insulin Sensitive from Insulin Resistant Obesity?

Xu, X Julia / Valentine, Rudy J / Ruderman, Neil B

Current obesity reports

2014 Volume 3, Issue 2, Page(s) 248–255

Abstract: Although a correlation exists between obesity and insulin resistance, roughly 25 % of obese individuals are insulin sensitive. AMP-activated protein kinase (AMPK) is a cellular energy sensor that among its many actions, integrates diverse physiological ... ...

Abstract	Although a correlation exists between obesity and insulin resistance, roughly 25 % of obese individuals are insulin sensitive. AMP-activated protein kinase (AMPK) is a cellular energy sensor that among its many actions, integrates diverse physiological signals to restore energy balance. In addition, in many situations it also increases insulin sensitivity. In this context, AMPK activity is decreased in very obese individuals undergoing bariatric surgery who are insulin resistant compared to equally obese patients who are insulin sensitive. In this review, we will both explore what distinguishes these individuals, and evaluate the evidence that diminished AMPK is associated with insulin resistance and metabolic syndrome-associated disorders in other circumstances.
Language	English
Publishing date	2014-05-07
Publishing country	United States
Document type	Journal Article
ISSN	2162-4968
ISSN (online)	2162-4968
DOI	10.1007/s13679-014-0095-x
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Article ; Online: Knockdown of GSK3β increases basal autophagy and AMPK signalling in nutrient-laden human aortic endothelial cells.

Weikel, Karen A / Cacicedo, José M / Ruderman, Neil B / Ido, Yasuo

Bioscience reports

2016 Volume 36, Issue 5

Abstract: High concentrations of glucose and palmitate increase endothelial cell inflammation and apoptosis, events that often precede atherogenesis. They may do so by decreasing basal autophagy and AMP-activated protein kinase (AMPK) activity, although the ... ...

Abstract	High concentrations of glucose and palmitate increase endothelial cell inflammation and apoptosis, events that often precede atherogenesis. They may do so by decreasing basal autophagy and AMP-activated protein kinase (AMPK) activity, although the mechanisms by which this occurs are not clear. Decreased function of the lysosome, an organelle required for autophagy and AMPK, have been associated with hyperactivity of glycogen synthase kinase 3β (GSK3β). To determine whether GSK3β affects nutrient-induced changes in autophagy and AMPK activity, we used a primary human aortic endothelial cell (HAEC) model of type 2 diabetes that we had previously characterized with impaired AMPK activity and autophagy [Weikel et al. (2015) Am. J. Phys. Cell Physiol. 308: , C249-C263]. Presently, we found that incubation of HAECs with excess nutrients (25 mM glucose and 0.4 mM palmitate) increased GSK3β activity and impaired lysosome acidification. Suppression of GSK3β in these cells by treatment with a chemical inhibitor or overexpression of kinase-dead GSK3β attenuated these lysosomal changes. Under control and excess nutrient conditions, knockdown of GSK3β increased autophagosome formation, forkhead box protein O1 (FOXO1) activity and AMPK signalling and decreased Akt signalling. Similar changes in autophagy, AMPK and Akt signalling were observed in aortas from mice treated with the GSK3β inhibitor CHIR 99021. Thus, increasing basal autophagy and AMPK activity by inhibiting GSK3β may be an effective strategy in the setting of hyperglycaemia and dyslipidaemia for restoring endothelial cell health and reducing atherogenesis.
Language	English
Publishing date	2016-10
Publishing country	England
Document type	Journal Article
ZDB-ID	764946-0
ISSN	1573-4935 ; 0144-8463
ISSN (online)	1573-4935
ISSN	0144-8463
DOI	10.1042/BSR20160174
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Article ; Online: Intensive insulin for type 2 diabetes: the risk of causing harm.

Nolan, Christopher J / Ruderman, Neil B / Prentki, Marc

The lancet. Diabetes & endocrinology

2013 Volume 1, Issue 1, Page(s) 9–10

MeSH term(s)	Animals ; Clinical Trials as Topic/methods ; Diabetes Mellitus, Type 2/blood ; Diabetes Mellitus, Type 2/drug therapy ; Humans ; Hypoglycemic Agents/administration & dosage ; Hypoglycemic Agents/adverse effects ; Insulin/administration & dosage ; Insulin/adverse effects ; Insulin Resistance/physiology ; Risk Factors
Chemical Substances	Hypoglycemic Agents ; Insulin
Language	English
Publishing date	2013-09
Publishing country	England
Document type	Journal Article ; Review
ISSN	2213-8595
ISSN (online)	2213-8595
DOI	10.1016/S2213-8587(13)70027-5
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Article ; Online: Adipose tissue inflammation and insulin resistance: all obese humans are not created equal.

Gauthier, Marie-Soleil / Ruderman, Neil B

The Biochemical journal

2010 Volume 430, Issue 2, Page(s) e1–4

Abstract: In recent years, it has become widely accepted that obesity is characterized by a chronic low-grade inflammation of adipose tissue that predisposes affected individuals to insulin resistance, Type 2 diabetes and other disorders associated with the ... ...

Abstract	In recent years, it has become widely accepted that obesity is characterized by a chronic low-grade inflammation of adipose tissue that predisposes affected individuals to insulin resistance, Type 2 diabetes and other disorders associated with the metabolic syndrome. On the other hand, a subset of obese individuals appears to be protected against insulin resistance and the disorders to which it predisposes. The comparison between such insulin-sensitive and insulin-resistant obese individuals offers a unique opportunity to identify key factors that either contribute to or prevent the development of insulin resistance in humans, without the confounding effect of a major difference in fat mass. In the previous issue of the Biochemical Journal, Barbarroja et al. reported that insulin-sensitive obese individuals show less inflammation in their visceral adipose tissue than a group of insulin-resistant subjects matched for BMI (body mass index). This finding reinforces the concept that inflammation in adipose tissue may be a cause of insulin resistance in most obese individuals, although it does not prove it. Further studies will be required for this purpose, as well as to identify the pathogenetic factors that determine whether or not adipose tissue of an obese individual becomes inflamed.
MeSH term(s)	Humans ; Insulin Resistance ; Intra-Abdominal Fat/immunology ; Intra-Abdominal Fat/metabolism ; Obesity/immunology ; Obesity/metabolism
Language	English
Publishing date	2010-09-01
Publishing country	England
Document type	Comment ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2969-5
ISSN	1470-8728 ; 0006-2936 ; 0306-3275 ; 0264-6021
ISSN (online)	1470-8728
ISSN	0006-2936 ; 0306-3275 ; 0264-6021
DOI	10.1042/BJ20101062
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Article: Nutrient Excess in AMPK Downregulation and Insulin Resistance.

Coughlan, Kimberly A / Valentine, Rudy J / Ruderman, Neil B / Saha, Asish K

Journal of endocrinology, diabetes & obesity

2015 Volume 1, Issue 1, Page(s) 1008

Abstract: It is well established that chronic exposure to excess nutrients leads to insulin resistance (IR) in skeletal muscle. Since skeletal muscle is responsible for 70-80% of insulin-stimulated glucose uptake, skeletal muscle IR is a key pathological component ...

Abstract	It is well established that chronic exposure to excess nutrients leads to insulin resistance (IR) in skeletal muscle. Since skeletal muscle is responsible for 70-80% of insulin-stimulated glucose uptake, skeletal muscle IR is a key pathological component of type 2 diabetes (T2D). Recent evidence suggests that inhibition of the nutrient-sensing enzyme AMP-activated protein kinase (AMPK) is an early event in the development of IR in response to high glucose, branched chain amino acids (BCAA), or fatty acids (FA). Whether the decrease in AMPK activity is causal to the events leading to insulin resistance (increased mTOR/p70S6K signaling) remains to be determined. Interestingly, pharmacological activation of AMPK can prevent activation of mTOR/p70S6K and insulin resistance, while inhibition of mTOR with rapamycin prevents insulin resistance, but not AMPK downregulation. AMPK can be inhibited by increased energy state (reduced AMP/ATP ratio), decreased phosphorylation of its activation site (αThr172) (by decreased upstream kinase activity or increased phosphatase activity), increased inhibitory phosphorylation at αSer485/491, changes in redox state or hormone levels, or other yet to be identified mechanisms. Excess nutrients also lead to an accumulation of the toxic lipid intermediates diacylglycerol (DAG) and ceramides, both of which can activate various protein kinase C (PKC) isoforms, and contribute to IR. The mechanism responsible for the initial downregulation of AMPK in response to excess nutrients, and whether glucose, BCAA, and FA act through similar or different pathways requires further study. Identification of this mechanism and the relative importance of other events would be beneficial for designing novel pharmacological interventions to prevent and/or reverse IR. This review will focus on the some of the mechanisms responsible for AMPK downregulation and the relative sequence and importance of these events.
Language	English
Publishing date	2015-07-02
Publishing country	United States
Document type	Journal Article
ISSN	2333-6692
ISSN	2333-6692
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Article ; Online: AMPK and the biochemistry of exercise: implications for human health and disease.

Richter, Erik A / Ruderman, Neil B

The Biochemical journal

2009 Volume 418, Issue 2, Page(s) 261–275

Abstract: AMPK (AMP-activated protein kinase) is a phylogenetically conserved fuel-sensing enzyme that is present in all mammalian cells. During exercise, it is activated in skeletal muscle in humans, and at least in rodents, also in adipose tissue, liver and ... ...

Abstract	AMPK (AMP-activated protein kinase) is a phylogenetically conserved fuel-sensing enzyme that is present in all mammalian cells. During exercise, it is activated in skeletal muscle in humans, and at least in rodents, also in adipose tissue, liver and perhaps other organs by events that increase the AMP/ATP ratio. When activated, AMPK stimulates energy-generating processes such as glucose uptake and fatty acid oxidation and decreases energy-consuming processes such as protein and lipid synthesis. Exercise is perhaps the most powerful physiological activator of AMPK and a unique model for studying its many physiological roles. In addition, it improves the metabolic status of rodents with a metabolic syndrome phenotype, as does treatment with AMPK-activating agents; it is therefore tempting to attribute the therapeutic benefits of regular physical activity to activation of AMPK. Here we review the acute and chronic effects of exercise on AMPK activity in skeletal muscle and other tissues. We also discuss the potential role of AMPK activation in mediating the prevention and treatment by exercise of specific disorders associated with the metabolic syndrome, including Type 2 diabetes and Alzheimer's disease.
MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; AMP-Activated Protein Kinases/physiology ; Animals ; Biomarkers/metabolism ; Disease/etiology ; Exercise/physiology ; Health ; Humans ; Models, Biological ; Motor Activity/physiology ; Muscle Contraction/physiology ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/physiology ; Time Factors
Chemical Substances	Biomarkers ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2009-01-22
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2969-5
ISSN	1470-8728 ; 0006-2936 ; 0306-3275 ; 0264-6021
ISSN (online)	1470-8728
ISSN	0006-2936 ; 0306-3275 ; 0264-6021
DOI	10.1042/BJ20082055
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Article ; Online: Response to Comments on Nolan et al. Insulin Resistance as a Physiological Defense Against Metabolic Stress: Implications for the Management of Subsets of Type 2 Diabetes. Diabetes 2015;64:673-686.

Nolan, Christopher J / Ruderman, Neil B / Kahn, Steven E / Pedersen, Oluf / Prentki, Marc

Diabetes

2015 Volume 64, Issue 10, Page(s) e38–9

MeSH term(s)	Diabetes Mellitus, Type 2/metabolism ; Humans ; Insulin Resistance/physiology ; Stress, Physiological/drug effects
Language	English
Publishing date	2015-10
Publishing country	United States
Document type	Comment ; Letter
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/dbi15-0002
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Article ; Online: Protocol for an evaluation of the initiation of an integrated longitudinal outpatient care model for severe chronic non-communicable diseases (PEN-Plus) at secondary care facilities (district hospitals) in 10 lower-income countries.

Adler, Alma J / Wroe, Emily B / Atzori, Andrea / Bay, Neusa / Bekele, Wondu / Bhambhani, Victoria M / Nkwiro, Remy Bitwayiki / Boudreaux, Chantelle / Calixte, Dawson / Chiwanda Banda, Jonathan / Coates, Matthew M / Dagnaw, Wubaye Walelgne / Domingues, Katia / Drown, Laura / Dusabeyezu, Symaque / Fenelon, Darius / Gupta, Neil / Ssinabulya, Isaac / Jain, Yogesh /

Kalkonde, Yogeshwar / Kamali, Innocent / Karekezi, Catherine / Karmacharya, Biraj Man / Koirala, Bhagawan / Makani, Julie / Manenti, Fabio / Mangwiro, Alexio / Manuel, Beatriz / Masiye, Jones K / Goma, Fastone Mathew / Mayige, Mary Theodory / McLaughlin, Amy / Mensah, Emmanuel / Salipa, Nicole Mocumbi / Mutagaywa, Reuben / Mutengerere, Alvern / Ngoga, Gedeon / Patiño, Marta / Putoto, Giovanni / Ruderman, Todd / Salvi, Devashri / Sesay, Santigie / Taero, Fameti / Tostão, Emílio / Toussaint, Sterman / Bukhman, Gene / Mocumbi, Ana Olga

BMJ open

2024 Volume 14, Issue 1, Page(s) e074182

Abstract: Introduction: The Package of Essential Noncommunicable Disease Interventions-Plus (PEN-Plus) is a strategy decentralising care for severe non-communicable diseases (NCDs) including type 1 diabetes, rheumatic heart disease and sickle cell disease, to ... ...

Abstract	Introduction: The Package of Essential Noncommunicable Disease Interventions-Plus (PEN-Plus) is a strategy decentralising care for severe non-communicable diseases (NCDs) including type 1 diabetes, rheumatic heart disease and sickle cell disease, to increase access to care. In the PEN-Plus model, mid-level clinicians in intermediary facilities in low and lower middle income countries are trained to provide integrated care for conditions where services traditionally were only available at tertiary referral facilities. For the upcoming phase of activities, 18 first-level hospitals in 9 countries and 1 state in India were selected for PEN-Plus expansion and will treat a variety of severe NCDs. Over 3 years, the countries and state are expected to: (1) establish PEN-Plus clinics in one or two district hospitals, (2) support these clinics to mature into training sites in preparation for national or state-level scale-up, and (3) work with the national or state-level stakeholders to describe, measure and advocate for PEN-Plus to support development of a national operational plan for scale-up. Methods and analysis: Guided by Proctor outcomes for implementation research, we are conducting a mixed-method evaluation consisting of 10 components to understand outcomes in clinical implementation, training and policy development. Data will be collected through a mix of quantitative surveys, routine reporting, routine clinical data and qualitative interviews. Ethics and dissemination: This protocol has been considered exempt or covered by central and local institutional review boards. Findings will be disseminated throughout the project's course, including through quarterly M&E discussions, semiannual formative assessments, dashboard mapping of progress, quarterly newsletters, regular feedback loops with national stakeholders and publication in peer-reviewed journals.
MeSH term(s)	Humans ; Noncommunicable Diseases/epidemiology ; Noncommunicable Diseases/therapy ; Hospitals, District ; Secondary Care Centers ; Ambulatory Care ; India/epidemiology
Language	English
Publishing date	2024-01-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2599832-8
ISSN	2044-6055 ; 2044-6055
ISSN (online)	2044-6055
ISSN	2044-6055
DOI	10.1136/bmjopen-2023-074182
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Article: AMPK activation: a therapeutic target for type 2 diabetes?

Coughlan, Kimberly A / Valentine, Rudy J / Ruderman, Neil B / Saha, Asish K

Diabetes, metabolic syndrome and obesity : targets and therapy

2014 Volume 7, Page(s) 241–253

Abstract: Type 2 diabetes (T2D) is a metabolic disease characterized by insulin resistance, β-cell dysfunction, and elevated hepatic glucose output. Over 350 million people worldwide have T2D, and the International Diabetes Federation projects that this number ... ...

Abstract	Type 2 diabetes (T2D) is a metabolic disease characterized by insulin resistance, β-cell dysfunction, and elevated hepatic glucose output. Over 350 million people worldwide have T2D, and the International Diabetes Federation projects that this number will increase to nearly 600 million by 2035. There is a great need for more effective treatments for maintaining glucose homeostasis and improving insulin sensitivity. AMP-activated protein kinase (AMPK) is an evolutionarily conserved serine/threonine kinase whose activation elicits insulin-sensitizing effects, making it an ideal therapeutic target for T2D. AMPK is an energy-sensing enzyme that is activated when cellular energy levels are low, and it signals to stimulate glucose uptake in skeletal muscles, fatty acid oxidation in adipose (and other) tissues, and reduces hepatic glucose production. There is substantial evidence suggesting that AMPK is dysregulated in animals and humans with metabolic syndrome or T2D, and that AMPK activation (physiological or pharmacological) can improve insulin sensitivity and metabolic health. Numerous pharmacological agents, natural compounds, and hormones are known to activate AMPK, either directly or indirectly - some of which (for example, metformin and thiazolidinediones) are currently used to treat T2D. This paper will review the regulation of the AMPK pathway and its role in T2D, some of the known AMPK activators and their mechanisms of action, and the potential for future improvements in targeting AMPK for the treatment of T2D.
Language	English
Publishing date	2014-06-24
Publishing country	New Zealand
Document type	Journal Article ; Review
ZDB-ID	2494854-8
ISSN	1178-7007
ISSN	1178-7007
DOI	10.2147/DMSO.S43731
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