Elevated Blood Lactate Is Not a Primary Cause of Anorexia in Tumor-Bearing Rats

Chance, William T.; Dayal, Ramesh; Friend, Lou Ann; James, J. Howard

doi:10.1207/s15327914nc4802_7

Cited by 4 publications

(11 citation statements)

References 53 publications

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“…Lactate levels increase in tumour‐bearing animals but not in pair‐fed animals . In tumour‐bearing animals, lactate levels increased contiguously with the onset of anorexia . Lactate infusion was associated with elevated levels of NPY in the ventromedial hypothalamus and dorsomedial hypothalamus, but there was no alteration in CRF.…”

Section: Lactatementioning

confidence: 88%

“… 64 In tumour-bearing animals, lactate levels increased contiguously with the onset of anorexia. 65 Lactate infusion was associated with elevated levels of NPY in the ventromedial hypothalamus and dorsomedial hypothalamus, but there was no alteration in CRF. Lactate suppresses food intake by activating adenosine monophosphate (AMP) kinase/methylmalonyl CoA signalling pathway 66 ( Figure 3 ).…”

Section: Lactatementioning

confidence: 89%

“…Dichloroacetate enhances pyruvate dehydrogenase, leading to a reduction of lactate. Dichloroacetate failed to decrease anorexia in tumour‐bearing rats . This may be due to conflicting effects of dichloroacetate on central levels of lactate.…”

Section: Lactatementioning

confidence: 97%

“…Dichloroacetate failed to decrease anorexia in tumour-bearing rats. 65 This may be due to conflicting effects of dichloroacetate on central levels of lactate.…”

Section: Lactatementioning

confidence: 99%

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Pathophysiology of anorexia in the cancer cachexia syndrome

Ezeoke

Morley

2015

Journal of Cachexia, Sarcopenia and Muscle

169

117

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Anorexia is commonly present in persons with cancer and a major component of cancer cachexia. There are multiple causes of anorexia in cancer. Peripherally, these can be due to (i) substances released from or by the tumour, e.g. pro-inflammatory cytokines, lactate, and parathormone-related peptide; (ii) tumours causing dysphagia or altering gut function; (iii) tumours altering nutrients, e.g. zinc deficiency; (iv) tumours causing hypoxia; (v) increased peripheral tryptophan leading to increased central serotonin; or (vi) alterations of release of peripheral hormones that alter feeding, e.g. peptide tyrosine tyrosine and ghrelin. Central effects include depression and pain, decreasing the desire to eat. Within the central nervous system, tumours create multiple alterations in neurotransmitters, neuropeptides, and prostaglandins that modulate feeding. Many of these neurotransmitters appear to produce their anorectic effects through the adenosine monophosphate kinase/methylmalonyl coenzyme A/fatty acid system in the hypothalamus. Dynamin is a guanosine triphosphatase that is responsible for internalization of melanocortin 4 receptors and prostaglandin receptors. Dynamin is up-regulated in a mouse model of cancer anorexia. A number of drugs, e.g. megestrol acetate, cannabinoids, and ghrelin agonists, have been shown to have some ability to be orexigenic in cancer patients.

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Section: Lactatementioning

confidence: 88%

Section: Lactatementioning

confidence: 89%

Section: Lactatementioning

confidence: 97%

“…Dichloroacetate failed to decrease anorexia in tumour-bearing rats. 65 This may be due to conflicting effects of dichloroacetate on central levels of lactate.…”

Section: Lactatementioning

confidence: 99%

See 2 more Smart Citations

Pathophysiology of anorexia in the cancer cachexia syndrome

Ezeoke

Morley

2015

Journal of Cachexia, Sarcopenia and Muscle

169

117

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“…Lactate's mechanism of action on orexigenic cells is via its effects on the adenosine monophosphate kinase/methylmalonyl CoA signaling pathway within the hypothalamus [103] . Lactate alone, however, does not seem to be responsible for cancer-associated anorexia (discussed below) [104] .…”

Section: Energy Balance and Feedingmentioning

confidence: 99%

Central regulation of breast cancer growth and metastasis

Borniger

2019

JCMT

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Cancer is a systemic disease. In order to fully understand it, we must take a holistic view on how cancer interacts with its host. The brain monitors and responds to natural and aberrant signals arriving from the periphery, particularly those of metabolic or immune origin. As has been well described, a hallmark of cancer is marked disruption of metabolic and inflammatory processes. Depending on the salience and timing of these inputs, the brain responds via neural and humoral routes to alter whole-body physiology. These responses have consequences for tumor growth and metastasis, directly influencing patient quality of life and subsequent mortality. Additionally, environmental inputs such as light, diet, and stress, can promote inappropriate neural activity that benefits cancer. Here, I discuss evidence for brain-tumor interactions, with special emphasis on subcortical neuromodulator neural populations, and potential ways of harnessing this cross-talk as a novel approach for cancer treatment.

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NMR- and MS-Based Untargeted Metabolomic Study of Stool and Serum Samples from Patients with Anorexia Nervosa

et al. 2021

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Anorexia nervosa (AN), a pathological restriction of food intake, leads to metabolic dysregulation. We conducted a metabolomics study to reveal changes caused by AN and the effect of hospital realimentation on metabolism. Both stool and serum from patients with AN and healthy controls were analyzed by NMR and MS. Statistical analysis revealed several altered biochemical and anthropometric parameters and 50 changed metabolites, including phospholipids, acylcarnitines, amino acids, derivatives of nicotinic acid, nucleotides, and energy metabolism intermediates. Biochemical and anthropometric parameters were correlated with metabolomic data. Metabolic changes in patients with AN described in our study imply serious system disruption defects, such as the development of inflammation and oxidative stress, changed free thyroxine (fT4) and thyroid-stimulating hormone (TSH) levels, a deficit of vitamins, muscle mass breakdown, and a decrease in ketone bodies as an important source of energy for the brain and heart. Furthermore, our data indicate only a very slight improvement after treatment. However, correlations of metabolomic results with body weight, interleukin 6, tumor necrosis factor α, fT4, and TSH might entail better prognoses and treatment effectiveness in patients with better system parameter status. Data sets are deposited in MassIVE: MSV000087713,

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Elevated Blood Lactate Is Not a Primary Cause of Anorexia in Tumor-Bearing Rats

Cited by 4 publications

References 53 publications

Pathophysiology of anorexia in the cancer cachexia syndrome

Pathophysiology of anorexia in the cancer cachexia syndrome

Central regulation of breast cancer growth and metastasis

NMR- and MS-Based Untargeted Metabolomic Study of Stool and Serum Samples from Patients with Anorexia Nervosa

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