Emerging Role of AMPK in Brown and Beige Adipose Tissue (BAT): Implications for Obesity, Insulin Resistance, and Type 2 Diabetes

Desjardins, Eric M.; Steinberg, Gregory R.

doi:10.1007/s11892-018-1049-6

Cited by 152 publications

(130 citation statements)

References 78 publications

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“…The ACE is critical in the generation of angiotensin II (AngII) [71], it plays the main role in the classic RAS pathway [72]. AMPK has been proved to associate with many kinds of diseases, for instance cardiovascular disease [9,63], metabolic syndrome [56,67], renal pathophysiology [73], and aging [44]. So there should be some association between ACE and AMPK.…”

Section: Ace and Ampkmentioning

confidence: 99%

AMPK: a balancer of the renin–angiotensin system

Liu

et al. 2019

Bioscience Reports

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The renin–angiotensin system (RAS) is undisputedly well-studied as one of the oldest and most critical regulators for arterial blood pressure, fluid volume, as well as renal function. In recent studies, RAS has also been implicated in the development of obesity, diabetes, hyperlipidemia, and other diseases, and also involved in the regulation of several signaling pathways such as proliferation, apoptosis and autophagy, and insulin resistance. AMP-activated protein kinase (AMPK), an essential cellular energy sensor, has also been discovered to be involved in these diseases and cellular pathways. This would imply a connection between the RAS and AMPK. Therefore, this review serves to draw attention to the cross-talk between RAS and AMPK, then summering the most recent literature which highlights AMPK as a point of balance between physiological and pathological functions of the RAS.

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Section: Ace and Ampkmentioning

confidence: 99%

AMPK: a balancer of the renin–angiotensin system

Liu

et al. 2019

Bioscience Reports

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“…AMPK stimulates the catabolic pathways to generate ATP while conserving the remaining ATP by switching off the anabolic pathways [99]. AMPK stimulates energy expenditure [29,[100][101][102][103][104][105][106][107][108][109], which maintains normal body weight, insulin sensitivity and liver-metabolism [103,[110][111][112][113][114][115][116][117]. Deregulation of AMPK is observed in obesity, diabetes and other metabolic diseases [29,[100][101][102][103][104][105][106][107][108][109][110][111][112][113][114][115]117].…”

Section: Bone Marrow Stem Cellsmentioning

confidence: 99%

“…Conversely, AMPK inhibits fatty acid biosynthesis, lipogenesis, cholesterol synthesis and gluconeogenesis by modulating ACC, sterol regulatory element binding protein 1C (SREBP1C), 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) and CREB-regulated transcription co-activator 2 (CRTC2) or forkhead box transcription factors (FoxO1), respectively [99]. Moreover, AMPK promotes adipose tissue browning mediated thermogenic energy expenditure [116]. For example, various agents like apelin, miRNA-455, resveratrol, cryptotanshinone, medicarpin and AICAR increase AMPK activity and adipocyte browning [116].…”

Section: Bone Marrow Stem Cellsmentioning

confidence: 99%

Targeting the Inositol Pyrophosphate Biosynthetic Enzymes in Metabolic Diseases

2020

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In mammals, a family of three inositol hexakisphosphate kinases (IP6Ks) synthesizes the inositol pyrophosphate 5-IP7 from IP6. Genetic deletion of Ip6k1 protects mice from high fat diet induced obesity, insulin resistance and fatty liver. IP6K1 generated 5-IP7 promotes insulin secretion from pancreatic β-cells, whereas it reduces insulin signaling in metabolic tissues by inhibiting the protein kinase Akt. Thus, IP6K1 promotes high fat diet induced hyperinsulinemia and insulin resistance in mice while its deletion has the opposite effects. IP6K1 also promotes fat accumulation in the adipose tissue by inhibiting the protein kinase AMPK mediated energy expenditure. Genetic deletion of Ip6k3 protects mice from age induced fat accumulation and insulin resistance. Accordingly, the pan IP6K inhibitor TNP [N2-(m-trifluorobenzyl), N6-(p-nitrobenzyl)purine] ameliorates obesity, insulin resistance and fatty liver in diet induced obese mice by improving Akt and AMPK mediated insulin sensitivity and energy expenditure. TNP also protects mice from bone loss, myocardial infarction and ischemia reperfusion injury. Thus, the IP6K pathway is a potential target in obesity and other metabolic diseases. Here, we summarize the studies that established IP6Ks as a potential target in metabolic diseases. Further studies will reveal whether inhibition of this pathway has similar pleiotropic benefits on metabolic health of humans.

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“…Therefore, the protein is a key therapeutic target for the treatment of major metabolic disorders including obesity and type-2 diabetes [103]. As adipogenesis is an energy consuming process, AMPK regulates the inhibition of expression of FAS, adipocyte specific pre-adipocytes, highlighting the potential role of AMPK in the inhibition of adipogenesis [111] In addition, AMPK has also been shown to be pertinent in the britening of WAT thereby increasing the energy expenditure through thermogenesis [112,113]. It has also been reported that the activity of AMPK increases during the differentiation of brown adipocytes and that targeting AMPK by short interfering RNAs (siRNAs), inhibits the differentiation of pre-adipocytes into mature brown adipocytes [16,114].…”

Section: Metabolic Functions Of Ampk and Role In Adipogenesismentioning

confidence: 99%

“…Upstream kinases of AMPK include Liver Kinase B1 (LKB1), mouse protein 25 (MO25) and STE-related adaptor (STRAD). LKB1[112,118], is part of a heterotrimeric protein.For activation, it needs the binding of other two upstream kinases of AMPK, STRAD and MO25 to form a heterotrimeric complex. It directly activates AMPK by phosphorylating Thr172 of α subunit.…”

mentioning

confidence: 99%

Molecular Mechanisms of Adipogenesis: The Anti-Obesogenic Role of AMP-Activated Protein Kinase and Recently Reported Plant Products

Ahmad¹,

Serpell²,

Lim³

et al. 2019

Preprint

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The Abnormal increase in the mass of adipose tissue during adipogenesis results in obesity. Obesity is a predominant disorder and its widespread has become a critical concern worldwide. This is due to the burden of its associated co-morbidities like cancer, cardiovascular diseases and diabetes. Over-nutrition and the sedentary lifestyle are considered as the most significant causes of abnormal adipose tissue development. Appropriate lifestyle and behavioural interventions are the corner stones of successful weight loss, but to maintain such a lifestyle is highly challenging. Accordingly, natural products from plants either as crude extracts or purified phytochemicals have shown to have anti-obesogenic properties and are generally non-toxic and cost-effective. In this review, we discuss the comparative analysis of molecular mechanisms involved in adipogenesis and the recently reported anti-obesogenic effects of various plant products. We will provide a common platform for understanding obesity and adipogenesis, and a possible mechanism of action for anti-obesogenic plant products through AMP-activated protein kinase (AMPK), which will support the scientific development of traditional herbal medicine.

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Emerging Role of AMPK in Brown and Beige Adipose Tissue (BAT): Implications for Obesity, Insulin Resistance, and Type 2 Diabetes

Cited by 152 publications

References 78 publications

AMPK: a balancer of the renin–angiotensin system

AMPK: a balancer of the renin–angiotensin system

Targeting the Inositol Pyrophosphate Biosynthetic Enzymes in Metabolic Diseases

Molecular Mechanisms of Adipogenesis: The Anti-Obesogenic Role of AMP-Activated Protein Kinase and Recently Reported Plant Products

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