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Hypothalamic Neuronal Circuits Are Modulated by Insulin and Impact Metabolism 1
Published in André Kleinridders, Physiological Consequences of Brain Insulin Action, 2023
Tadeu de Oliveira Diz, Sabela Casado, Rubén Nogueiras, Sulay Tovar
Brain insulin resistance seems to be due to an inflammatory process in the hypothalamus, where insulin receptors are expressed at high density. This impairs local signalling systems by inducing mitochondrial dysfunction and endoplasmic reticulum stress in the hypothalamus, and cause glucose and energy metabolism disorders. Through studies with obesity models induced by a high-fat diet, it was observed that animals submitted to this type of diet, presented an inflammatory process and decreased sensitivity to insulin in the hypothalamus (200–202). Insulin resistance in most cases is believed to be manifest at the cellular level via post-receptor defects in insulin signalling. Possible mechanisms include down-regulation, deficiencies, or genetic polymorphisms of tyrosine phosphorylation of the insulin receptor, IRS proteins or PIP-3 kinase, or may involve abnormalities of glucose transporter type 4 function (203). Despite promising findings in experimental animals with respect to a range of insulin signalling defects, their relevance to human insulin resistance is presently unclear.
Extensor tendon injuries
Published in Peter Houpt, Hand Injuries in the Emergency Department, 2023
In the acute phase, the patient experiences pain at the level of the PIP joint. In a closed rupture there is swelling on the dorsal side where sometimes the avulsed central slip is palpable. If examined carefully, a slight extension deficit is noted. The Elson test is performed; ask the patient to bend the PIP joint 90° over the edge of the table and extend the middle phalanx against resistance. In presence of central slip injury there will be a weak PIP extension and a rigid DIP (due to pulling of the lateral slips). Closed injury require X-ray investigation in two directions to exclude an avulsion fracture.
Neuropeptide Regulation of Ion Channels and Food Intake
Published in Tian-Le Xu, Long-Jun Wu, Nonclassical Ion Channels in the Nervous System, 2021
Ion channels tightly control the neuronal activity through transmembrane ion flux for depolarization or hyperpolarization. Changes in the protein structure of ion channels can drastically change how the neuron responds to extracellular signals such as neuropeptides. For instance, dysfunctional KATP channels, possibly from high-fat diets, would be unable to close under elevated glucose levels, resulting in constitutively active inhibition of the anorexigenic POMC neurons, leading to the development of obesity (Parton et al. 2007). Mutations in KATP channels are also associated with congenital diabetes and hyperinsulinism (Tinker et al. 2018). Tonically elevated PIP3, a signaling molecule naturally activated by insulin, acts as a sexually dimorphic inhibitor of POMC neurons via stimulation of KATP channels. Female mice have a larger weight gain than males when PIP3 is perpetually elevated (Plum et al. 2006). Kir6.2 is a key pore-forming subunit of KATP channels (Miki et al. 2001). The defective Kir6.2 prevents ATP blockade of KATP channels, which results in increased food intake and obesity due to loss of glucose sensitivity of Kir6.2-expressing hypothalamic neurons (Sohn 2013; Miki et al. 2001). Kir6.2 knockout mice also showed a blunted hypothalamic response to glucose loading and elevated hypothalamic NPY expression accompanied by hyperphagia, while they are resistant to obesity (Park et al. 2011).
Protein markers of spermatogenesis and their potential use in the management of azoospermia
Published in Expert Review of Proteomics, 2021
Sophia Costa Araujo, Ricardo Pimenta Bertolla
Prolactin-inducible protein (PIP) is expressed in various exocrine tissues, such as lacrimal, salivary, sweat glands, and in seminal vesicles. Its expression is up-regulated by prolactin and androgens, and it is down-regulated by estrogens. The exact role of PIP in male fertility and infertility remains unknown, so several studies have been performed to interpret its relationship to male infertility. Published studies show that this protein has the potential to reflect and predict seminal alterations. PIP is considered a strong prognostic biomarker in metastatic breast and prostate cancer, due to its overexpression in them. Furthermore, its aspartyl-proteinase nature also suggests its role in tumor progression [102]. A study by Yamakawa et al. [5] showed that PIP was absent in all samples from patients with OA and absent in samples from some patients with NOA. Suggesting that the origin of PIP is not only from the seminal vesicle, but also from the testis or epididymis.
Tear film, contact lenses and tear biomarkers
Published in Clinical and Experimental Optometry, 2019
Using radiolabelled peptides that differ in mass from the normal non‐labelled versions by known degrees, it is possible to quantify the amount of proteins of interest that are present in samples. This technique has been used to quantify the amount of lactoferrin,2014 lysozyme, lipocalin‐1 and, for the first time, the concentration of prolactin‐induced protein and proline‐rich protein‐4 in tears.2014 Immunoassays2001 including multiplex bead assays2015 also have been used to provide quantitative data for several proteins in one sample. Table 1 shows the concentration of some of the proteins we have been examining in tears.1996 The concentration of proteins in tears has a large dynamic range, from mg/ml for proteins such as lactoferrin and lysozyme to pg/ml for the interleukin inflammatory mediators.
Sperm DNA damage and its impact on male reproductive health: a critical review for clinicians, reproductive professionals and researchers
Published in Expert Review of Molecular Diagnostics, 2019
Ashok Agarwal, Manesh Kumar Panner Selvam, Saradha Baskaran, Chak-Lam Cho
Sperm morphological abnormality such as teratozoospermia and ultra-structural changes such as vacuolation in nucleus are associated with SDF [50]. Furthermore, the sperm functions such as hyperactivation, capacitation, and acrosome reaction, critical for the fertilization process, are defective in sperm with high DNA damage [51,52]. Both nuclear and mitochondria DNA damages are reflected on the molecular machinery at the subcellular level [53,54]. Sperm and seminal plasma proteome are altered in the patients with high SDF [55]. Molecular processes associated with energy production, protein folding, triacylglycerol metabolism, and cellular detoxification are dysregulated in the spermatozoa with high nuclear DNA fragmentation [54]. Spermatogenesis process is disrupted in men with high SDF due to alteration in the expression of prolactin induced protein and its precursor protein. In addition, proteins associated with DNA binding (such as sperm protein associated with nucleus in the X chromosome and histone proteins), OS, and mitochondrial functions were reported to be differentially expressed in men with high SDF [56]. Post-genomic pathways associated with sperm metabolism and function and protection against OS are also dysregulated in men having high SDF [54].