Expression of messenger RNA encoding two cellular metabolic regulators, AMP-activated protein kinase (AMPK) and O-GlcNAc transferase (OGT), in channel catfish: Their tissue distribution and relationship with changes in food intake

The knowledge regarding hypothalamic integration of metabolic and endocrine signaling resulting in regulation of food intake is scarce in fish. Available studies pointed to a network in which the activation of the nutrient-sensing (glucose, fatty acid, and amino acid) systems would result in AMP-activated protein kinase (AMPK) inhibition and activation of protein kinase B (Akt) and mechanistic target of rapamycin (mTOR). Changes in these signaling pathways would control phosphorylation of transcription factors cAMP response-element binding protein (CREB), forkhead box01 (FoxO1), and brain homeobox transcription factor (BSX) leading to food intake inhibition through changes in the expression of neuropeptide Y (NPY), agouti-related peptide (AgRP), pro-opio melanocortin (POMC), and cocaine and amphetamine-related transcript (CART). The present mini-review summarizes information on the topic and identifies gaps for future research.

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Hypothalamic AMP-activated Protein Kinase as a Regulator of Food Intake and Energy Balance

CNS & Neurological Disorders - Drug Targets ◽

10.2174/1871527315666160815165806 ◽

2016 ◽

Vol 15 (8) ◽

pp. 896-909 ◽

Cited By ~ 5

Author(s):

Tae Seok Oh ◽

Yoonjeong Jeon ◽

Seolsong Kim ◽

Eun-Kyoung Kim

Keyword(s):

Energy Balance ◽

Protein Kinase ◽

Food Intake ◽

Amp Activated Protein Kinase

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Faculty Opinions recommendation of AMP-activated protein kinase plays a role in the control of food intake.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1018602.210453 ◽

2004 ◽

Author(s):

Angus Nairn

Keyword(s):

Protein Kinase ◽

Food Intake ◽

Amp Activated Protein Kinase

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A Central Role for Neuronal Adenosine 5′-Monophosphate-Activated Protein Kinase in Cancer-Induced Anorexia

Endocrinology ◽

10.1210/en.2007-0381 ◽

2007 ◽

Vol 148 (11) ◽

pp. 5220-5229 ◽

Cited By ~ 35

Author(s):

Eduardo R. Ropelle ◽

José R. Pauli ◽

Karina G. Zecchin ◽

Mirian Ueno ◽

Cláudio T. de Souza ◽

...

Keyword(s):

Protein Kinase ◽

Food Intake ◽

Life Span ◽

Energy Homeostasis ◽

Ampk Activation ◽

Chronic Infusion ◽

The Central Nervous System ◽

Amp Activated Protein Kinase ◽

Oxide Synthase ◽

Cancer Anorexia

The pathogenesis of cancer anorexia is multifactorial and associated with disturbances of the central physiological mechanisms controlling food intake. However, the neurochemical mechanisms responsible for cancer-induced anorexia are unclear. Here we show that chronic infusion of 5-amino-4imidazolecarboxamide-riboside into the third cerebral ventricle and a chronic peripheral injection of 2 deoxy-d-glucose promotes hypothalamic AMP-activated protein kinase (AMPK) activation, increases food intake, and prolongs the survival of anorexic tumor-bearing (TB) rats. In parallel, the pharmacological activation of hypothalamic AMPK in TB animals markedly reduced the hypothalamic production of inducible nitric oxide synthase, IL-1β, and TNF-α and modulated the expression of proopiomelanocortin, a hypothalamic neuropeptide that is involved in the control of energy homeostasis. Furthermore, the daily oral and intracerebroventricular treatment with biguanide antidiabetic drug metformin also induced AMPK phosphorylation in the central nervous system and increased food intake and life span in anorexic TB rats. Collectively, the findings of this study suggest that hypothalamic AMPK activation reverses cancer anorexia by inhibiting the production of proinflammatory molecules and controlling the neuropeptide expression in the hypothalamus, reflecting in a prolonged life span in TB rats. Thus, our data indicate that hypothalamic AMPK activation presents an attractive opportunity for the treatment of cancer-induced anorexia.

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AMP-activated protein kinase activates neuropeptide Y neurons in the hypothalamic arcuate nucleus to increase food intake in rats

Neuroscience Letters ◽

10.1016/j.neulet.2011.05.060 ◽

2011 ◽

Vol 499 (3) ◽

pp. 194-198 ◽

Cited By ~ 33

Author(s):

Daisuke Kohno ◽

Hideyuki Sone ◽

Shigeyasu Tanaka ◽

Hideharu Kurita ◽

Darambazar Gantulga ◽

...

Keyword(s):

Protein Kinase ◽

Food Intake ◽

Neuropeptide Y ◽

Arcuate Nucleus ◽

Increase Food Intake ◽

Hypothalamic Arcuate Nucleus ◽

Amp Activated Protein Kinase

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Differential Effects of Acute and Chronic Estrogen Treatment on Thermogenic and Metabolic Pathways in Ovariectomized Sheep

Endocrinology ◽

10.1210/en.2012-1758 ◽

2013 ◽

Vol 154 (1) ◽

pp. 184-192 ◽

Cited By ~ 17

Author(s):

Scott D. Clarke ◽

Iain J. Clarke ◽

Alexandra Rao ◽

Roger G. Evans ◽

Belinda A. Henry

Keyword(s):

Skeletal Muscle ◽

Blood Flow ◽

Protein Kinase ◽

Food Intake ◽

Femoral Artery ◽

Heat Production ◽

Artery Blood Flow ◽

Femoral Artery Blood Flow ◽

Amp Activated Protein Kinase ◽

Estradiol 17Β

Estrogen is protective against weight gain, but the underlying mechanisms are not fully elucidated. We sought to characterize the effects of estrogen on energy expenditure in skeletal muscle and adipose tissue in ovariectomized sheep. Temperature probes were implanted into sc (gluteal) and visceral (retroperitoneal) fat depots and skeletal muscle of the hind limb (vastus lateralis). Food was available from 1100–1600 h to entrain postprandial thermogenesis. We characterized the effects of single (50 μg estradiol benzoate, im) and repeated (25 μg estradiol-17β, iv) injections as well as chronic (3 × 3 cm estradiol-17β implants for 7 d) treatment on heat production. A single injection of estrogen increased heat production in visceral fat and skeletal muscle, without an effect on food intake. Increased heat production in skeletal muscle was sustained by repeated estradiol-17β injections. On the other hand, continuous treatment reduced food intake but had no effect on thermogenesis. To determine possible mechanisms that underpin estradiol-17β-induced heat production, we measured femoral artery blood flow, the expression of uncoupling protein (UCP) mRNA and the phosphorylation of AMP-activated protein kinase and Akt in fat and muscle. There was little effect of either single or repeated injections of estradiol-17β on the expression of UCP1, -2, or -3 mRNA in visceral fat or skeletal muscle. Acute injection of estradiol-17β increased the phosphorylation of AMP-activated protein kinase and Akt in muscle only. Estradiol-17β treatment did not alter femoral artery blood flow. Thus, the stimulatory effect of estradiol-17β on thermogenesis in female sheep is dependent upon a pulsatile pattern of treatment and not constant continuous exposure.

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AICAR and Compound C regulate food intake independently of AMP-activated protein kinase in lines of chickens selected for high or low body weight

Comparative Biochemistry and Physiology Part A Molecular & Integrative Physiology ◽

10.1016/j.cbpa.2011.04.004 ◽

2011 ◽

Vol 159 (4) ◽

pp. 401-412 ◽

Cited By ~ 6

Author(s):

Pingwen Xu ◽

Paul B. Siegel ◽

D. Michael Denbow

Keyword(s):

Body Weight ◽

Protein Kinase ◽

Food Intake ◽

Compound C ◽

Regulate Food Intake ◽

Amp Activated Protein Kinase

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Palmitoylethanolamide Prevents Metabolic Alterations and Restores Leptin Sensitivity in Ovariectomized Rats

Endocrinology ◽

10.1210/en.2013-1823 ◽

2014 ◽

Vol 155 (4) ◽

pp. 1291-1301 ◽

Cited By ~ 27

Author(s):

G. Mattace Raso ◽

A. Santoro ◽

R. Russo ◽

R. Simeoli ◽

O. Paciello ◽

...

Keyword(s):

Body Weight ◽

Adipose Tissue ◽

Weight Gain ◽

Protein Kinase ◽

Food Intake ◽

Neuroblastoma Cell ◽

Ovariectomized Rats ◽

Leptin Signaling ◽

Leptin Sensitivity ◽

Amp Activated Protein Kinase

It has been suggested a role of fatty acid ethanolamides in control of feeding behavior. Among these, palmitoylethanolamide (PEA) has not been directly implicated in appetite regulation and weight gain. The aim of this study was to investigate the effect of PEA on food intake and body weight and the interaction between PEA and hypothalamic leptin signaling in ovariectomized rats. Ovariectomy produced hyperphagia and increased weight gain, making it an useful model of mild obesity. Ovariectomized rats were treated with PEA (30 mg/kg sc) for 5 weeks. Then, blood was collected, and hypothalamus and adipose tissue were removed for histological, cellular, and molecular measurements. We showed that PEA caused a reduction of food intake, body weight, and fat mass. The mechanisms underlying PEA effects involved an improvement in hypothalamic leptin signaling, through a raise in signal transducer and activator of transcription 3 phosphorylation. We also reported that PEA reduced AMP-activated protein kinase-α phosphorylation and modulated transcription of anorectic and orexigenic neuropeptides in the hypothalamus. Moreover, PEA increased AMP-activated protein kinase-α phosphorylation and carnitine palmitoyltransferase 1 transcription in adipose tissue, suggesting an increase in ATP-producing catabolic pathway. PEA also polarized adipose tissue macrophages to M2 lean phenotype, associated to a reduction of inflammatory cytokines/adipokines. To demonstrate the direct effect of PEA on leptin sensitivity without interference of adiposity loss, we obtained consistent data in PEA-treated sham-operated animals and in vitro in SH-SY5Y neuroblastoma cell line. Therefore, our data provide a rationale for the therapeutic use of PEA in obese postmenopausal woman.

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