Matangazo

Uzalishaji wa Glucose Upatanishi kwenye Ini unaweza Kudhibiti na Kuzuia Kisukari

An important marker for ugonjwa wa kisukari development has been identified.

Homoni mbili muhimu zinazozalishwa kwenye kongosho - glukoni na insulin - kudhibiti ipasavyo glucose viwango kulingana na chakula tunachotumia. Glucagon huongeza Uzalishaji wa Glucose ya Hepatic (HGP) na insulini hupunguza. Wote wawili hudhibiti homeostasis ya sukari ya damu. Tunapokuwa kwenye mfungo, glucagon hutolewa kutoka kwa seli za kongosho ili kuongeza sukari ya damu mwilini ili kulinda mwili kutokana na hali inayoitwa hypoglycaemia ambapo viwango vya sukari ya damu ya mtu hushuka sana na kusababisha dalili. Glucagon inahusika katika ukuzaji wa hyperglycemia ya kisukari wakati Uzalishaji wa Glucose ya Hepatic (HGP) unaongezeka. Insulini hukandamiza uzalishaji wa glukosi kupitia maandishi ya kawaida ndani ini cells. A protein called Transcription factor Foxo1 plays an important role in regulating expression of genes and promoting HGP by increasing expression of genes which are responsible for production of glucose. Disruption of proper HGP is understood as a key primary mechanism for development of Type 2 ugonjwa wa kisukari.

Katika utafiti uliochapishwa katika Kisukari, researchers from Texas A&M University USA set out to understand the role of Foxo1 in how glucagon regulates HGP. They wanted to better understand the fundamentals of blood glucose homeostasis and pathogenesis of diabetes. Glucagon does its function by binding to a GPCR receptor, stimulating the cell membrane to activate protein kinase A which then signals gene expression to increase blood glucose. The levels of glucagon are extremely high in humans with ugonjwa wa kisukari and this stimulates excess production of HGP.

Researchers investigated Foxo1 regulation through phosphorylation i.e. attachment of a phosphoryl group. Phosphorylation is an important part of protein function and is responsible for activating or deactivating almost 50 percent of enzymes present in our body, and thereby regulating their function. Researchers used mice model and gene editing to generate Foxo1 ‘knock in’ mice. Foxo1 was stabilised in ini of mice (who were fasting) when insulin was decreased and glucagon increased in the bloodstream. The study clearly showed that if hepatic Foxo1 was deleted, hepatic glucose production (HGP) and blood glucose was decreased in mice. Thus, a novel mechanism has been identified for the first time in which Foxo1 mediates glycogen signalling via phosphorylation in order to control blood glucose.

Foxo1 is an important protein that acts as a mediator for various pathways integrating hormones and other proteins to control insulin sensitivity. Since high glucagon levels are present both in Type 1 and Type 2 ugonjwa wa kisukari, Foxo1 will play an important role in the fundamental mechanism leading to diabetic hyperglycaemia. The study suggests that glucagon mediated HGP can be a potential therapeutic intervention for control and also possible prevention of ugonjwa wa kisukari.

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{Unaweza kusoma karatasi asili ya utafiti kwa kubofya kiungo cha DOI kilichotolewa hapa chini katika orodha ya (vyanzo) vilivyotajwa}

Chanzo (s)

Yuxin W et al. 2018. Utaratibu wa Riwaya ya Foxo1 Phosphorylation katika Glucagon Signaling in Control of Glucose Homeostasis.Kisukari. 67 (11). https://doi.org/10.2337/db18-0674

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