MicroRNAs in the hypothalamic control of energy homeostasis

Najam, Syeda Sadia; Zglinicki, Bartosz; Vinnikov, Ilya A.; Konopka, Witold

doi:10.1007/s00441-018-2876-0

Cited by 9 publications

(5 citation statements)

References 25 publications

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“…Certain microRNAs may turn out to be distinct or differentially expressed in ME/CFS. Recently, microRNAs have been implicated in the hypothalamic control of energy homeostasis (Najam et al, 2018). However, the available studies in patients with ME/CFS did not report any consistent pattern whether pre-or postexercise in plasma, (Brenu et al, 2014) natural killer cells (Petty et al, 2016), or CD8 1 cells (Brenu et al, 2012).…”

Section: Mitochondrial Dysfunctionmentioning

confidence: 97%

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome—Metabolic Disease or Disturbed Homeostasis due to Focal Inflammation in the Hypothalamus?

Hatziagelaki

Adamaki

Tsilioni

et al. 2018

J Pharmacol Exp Ther

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Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex disease characterized by debilitating fatigue, lasting for at least 6 months, with associated malaise, headaches, sleep disturbance, and cognitive impairment, which severely impacts quality of life. A significant percentage of ME/CFS patients remain undiagnosed, mainly due to the complexity of the disease and the lack of reliable objective biomarkers. ME/CFS patients display decreased metabolism and the severity of symptoms appears to be directly correlated to the degree of metabolic reduction that may be unique to each individual patient. However, the precise pathogenesis is still unknown, preventing the development of effective treatments. The ME/CFS phenotype has been associated with abnormalities in energy metabolism, which are apparently due to mitochondrial dysfunction in the absence of mitochondrial diseases, resulting in reduced oxidative metabolism. Such mitochondria may be further contributing to the ME/CFS symptomatology by extracellular secretion of mitochondrial DNA, which could act as an innate pathogen and create an autoinflammatory state in the hypothalamus. We propose that stimulation of hypothalamic mast cells by environmental, neuroimmune, pathogenic and stress triggers activates microglia, leading to focal inflammation in the brain and disturbed homeostasis. This process could be targeted for the development of novel effective treatments.

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Section: Mitochondrial Dysfunctionmentioning

confidence: 97%

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome—Metabolic Disease or Disturbed Homeostasis due to Focal Inflammation in the Hypothalamus?

Hatziagelaki

Adamaki

Tsilioni

et al. 2018

J Pharmacol Exp Ther

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“…The hypothalamus is vital in the modulation of energy homeostasis by regulating energy expenditure and food intake [129]. The hypothalamus is responsible for a broad spectrum of physiological functions, such as reproduction, water balance, regulation, metabolism and feeding, and cardiovascular function.…”

Section: Cognitive Impairment and Hypothalamic Inflammationmentioning

confidence: 99%

Effect of High-Fat Diets on Oxidative Stress, Cellular Inflammatory Response and Cognitive Function

2019

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Cognitive dysfunction is linked to chronic low-grade inflammatory stress that contributes to cell-mediated immunity in creating an oxidative environment. Food is a vitally important energy source; it affects brain function and provides direct energy. Several studies have indicated that high-fat consumption causes overproduction of circulating free fatty acids and systemic inflammation. Immune cells, free fatty acids, and circulating cytokines reach the hypothalamus and initiate local inflammation through processes such as microglial proliferation. Therefore, the role of high-fat diet (HFD) in promoting oxidative stress and neurodegeneration is worthy of further discussion. Of particular interest in this article, we highlight the associations and molecular mechanisms of HFD in the modulation of inflammation and cognitive deficits. Taken together, a better understanding of the role of oxidative stress in cognitive impairment following HFD consumption would provide a useful approach for the prevention of cognitive dysfunction.

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“…On the other – the appetite-suppressing (anorexigenic) neuronal population expresses Tbx3 [ 3 ] transcription factor and proopiomelanocortin (POMC), the precursor of α-melanocyte-stimulating hormone [ 4 ]. These neurons signal to various hypothalamic and extra-hypothalamic structures to control food intake and energy expenditure [ 5 ]. Reporter analyses in Tg (Pomc1-cre)16Lowl/J (JAX: 005965, further referred to as POMC Cre ) transgenic mouse line [ 6 ] revealed that all of the POMC-expressing precursor cells continue to express Tbx3 throughout the adulthood [ 3 ] .…”

Section: Introductionmentioning

confidence: 99%