A Comprehensive Review on GLP-1 Signaling Pathways in the Management of Diabetes Mellitus - Focus on the Potential Role of GLP-1 Receptors Agonists and Selenium Among Various Organ Systems.

Diabetes Mellitus develops when the body becomes unable to fuel its cells with glucose, which results in the accumulation of sugar excess in the bloodstream. Because it has diverse pathophysiological impacts on the body, diabetes mellitus represents a significant issue of concern in an attempt to find suitable treatment modalities and medications for afflicted diabetic patients. Glucagon-like peptide 1 (GLP-1) plays a pivotal role in the incretin effect, emerging as a prospective treatment for diabetes mellitus and a promising means of regenerating pancreatic cells, whether directly or through its receptor agonists. It has been shown that GLP-1 efficiently increases insulin production, lowers blood sugar levels in patients with type 2 diabetes mellitus, and decreases appetite, craving, and hunger, therefore amplifying the sensation of fullness and satiety. Moreover, since they are all dependent on GLP-1 effect, intricate signaling pathways share some similarities during specific phases, although the pathways continue to exhibit significant divergence engendered by specific reactions and effects in each organ, which encompasses the rationale behind observed differences. This triggers an expanding range of GLP-1 R agonists, creating new unforeseen research and therapeutic application prospects. This review aims to explain the incretin effect, discuss how GLP-1 regulates blood glucose levels, and how it affects different body organs, as well as how it transmits signals, before introducing selenium's role in the incretin impact.

Satiety: a gut-brain-relationship.

Many hormones act on the hypothalamus to control hunger and satiety through various pathways closely associated with several factors. When food is present in the gastro intestinal (GI) tract, enteroendocrine cells (EECs) emit satiety signals such as cholecystokinin (CCK), glucagon like peptide-1 (GLP-1) and peptide YY (PYY), which can then communicate with the vagus nerve to control food intake. More specifically, satiety has been shown to be particularly affected by the GLP-1 hormone and its receptor agonists that have lately been acknowledged as a promising way to reduce weight. In addition, there is increasing evidence that normal flora is also involved in the peripheral, central, and reward system that impact satiety. Moreover, neurologic pathways control satiety through neurotransmitters. In this review, we discuss the different roles of each of the GLP-1 hormone and its agonist, gut microbiomes, as well as neurotransmitters and their interconnected relation in the regulation of body's satiety homeostasis.

Mental Health: Pandemics, Epidemics and Tau Protein.

Background: It is well established that a wide range of psychological disorders are influenced by the way people live, with lifestyle-related factors playing a substantial role. During the past decade, the effects of major disasters on mental health have drawn a lot of attention. Aim: In this review, we compare clinical studies reporting a link between COVID-19 and other pandemics and mental health. Importantly, we also shed light on Tau protein and neurotransmitters as neurobiological factors that might explain this link. Methods: A thorough PubMed search was done to gather and summarize published data on the COVID-19 pandemic's effect on mental health. Additionally, these studies were compared to previous research published on PubMed, triggering other pandemic and epidemic impacts on mental health. Results: The COVID-19 epidemic has had the biggest impact on raising awareness about mental health. Moreover, the past century has seen an increase in the frequency of disease outbreaks like MERS-CoV, Ebola, and Influenza, which all had an impact on mental health. However, the exact role of these epidemics on mental health and brain functions is poorly understood. Conclusion: Future research on the underlying pathways may yield essential information for the treatment and prevention of prospective mental diseases in light of the ongoing decline in mental health during the past 10 years.

Arginine deprivation as a treatment approach targeting cancer cell metabolism and survival: A review of the literature.

Amino acid requirement of metabolically active cells is a key element in cellular survival. Of note, cancer cells were shown to have an abnormal metabolism and high-energy requirements including the high amino acid requirement needed for growth factor synthesis. Thus, amino acid deprivation is considered a novel approach to inhibit cancer cell proliferation and offer potential treatment prospects. Accordingly, arginine was proven to play a significant role in cancer cell metabolism and therapy. Arginine depletion induced cell death in various types of cancer cells. Also, the various mechanisms of arginine deprivation, e.g., apoptosis and autophagy were summarized. Finally, the adaptive mechanisms of arginine were also investigated. Several malignant tumors had high amino acid metabolic requirements to accommodate their rapid growth. Antimetabolites that prevent the production of amino acids were also developed as anticancer therapies and are currently under clinical investigation. The aim of this review is to provide a concise literature on arginine metabolism and deprivation, its effects in different tumors, its different modes of action, as well as the related cancerous escape mechanisms.

SARS-CoV-2-mediated liver injury: pathophysiology and mechanisms of disease.

BACKGROUND: SARS-CoV-2-induced severe inflammatory response can be associated with severe medical consequences leading to multi-organ failure, including the liver. The main mechanism behind this assault is the aggressive cytokine storm that induces cytotoxicity in various organs. Of interest, hepatic stellate cells (HSC) respond acutely to liver injury through several molecular mechanisms, hence furthering the perpetuation of the cytokine storm and its resultant tissue damage. In addition, hepatocytes undergo apoptosis or necrosis resulting in the release of pro-inflammatory and pro-fibrogenic mediators that lead to chronic liver inflammation. AIMS: The aim of this review is to summarize available data on SARS-CoV-2-induced liver inflammation in addition to evaluate the potential effect of anti-inflammatory drugs in attenuating SARS-CoV-2-induced liver inflammation. METHODS: Thorough PubMed search was done to gather and summarize published data on SARS-CoV-2-induced liver inflammation. Additionally, various anti-inflammatory potential treatments were also documented. RESULTS: Published data documented SARS-CoV-2 infection of liver tissues and is prominent in most liver cells. Also, histological analysis showed various features of tissues damage, e.g., hepatocellular necrosis, mitosis, cellular infiltration, and fatty degeneration in addition to microvesicular steatosis and inflammation. Finally, the efficacy of the different drugs used to treat SARS-CoV-2-induced liver injury, in particular the anti-inflammatory remedies, are likely to have some beneficial effect to treat liver injury in COVID-19. CONCLUSION: SARS-CoV-2-induced liver inflammation is a serious condition, and drugs with potent anti-inflammatory effect can play a major role in preventing irreversible liver damage in COVID-19.