Ny forskningsrapport - 4e för veckan

9 forskare från Fu Jen Catholic University, Taiwan har fått sina studier om obesity (övervikt) publicerade. 

Övervikt bland barn närmare bestämt. Studien är intressant då forskarna verkligen gått till botten med ev gemensam nämnare för barnfetma tidigare forskning inte kunnat hitta. Forskarna i denna studie tror dock att de funnit denna gemensamma nämnare. Men till studien :

Participation of lipopolysaccharide in hyperplasic adipose expansion: Involvement of NADPH oxidase/ROS/p42/p44 MAPK-dependent Cyclooxygenase-2

First published: 01 June 2022

Abstract

Obesity is a world-wide problem, especially the child obesity, with the complication of various metabolic diseases. Child obesity can be developed as early as the age between 2 and 6. The expansion of fat mass in child age includes both hyperplasia and hypertrophy of adipose tissue, suggesting the importance of proliferation and adipogenesis of preadipocytes. The changed composition of gut microbiota is associated with obesity, revealing the roles of lipopolysaccharide (LPS) on manipulating adipose tissue development. Studies suggest that LPS enters the circulation and acts as a pro-inflammatory regulator to facilitate pathologies. Nevertheless, the underlying mechanisms behind LPS-modulated obesity are yet clearly elucidated. This study showed that LPS enhanced the expression of cyclooxygenase-2 (COX-2), an inflammatory regulator of obesity, in preadipocytes. Pretreating preadipocytes with the scavenger of reactive oxygen species (ROS) or the inhibitors of NADPH oxidase or p42/p44 MAPK markedly decreased LPS-stimulated gene expression of COX-2 together with the phosphorylation of p47^phox and p42/p44 MAPK, separately. LPS activated p42/p44 MAPK via NADPH oxidase-dependent ROS accumulation in preadipocytes. Reduction of intracellular ROS or attenuation of p42/p44 MAPK activation both reduced LPS-mediated COX-2 expression and preadipocyte proliferation. Moreover, LPS-induced preadipocyte proliferation and adipogenesis were abolished by the inhibition of COX-2 or PEG₂ receptors. Taken together, our results suggested that LPS enhanced the proliferation and adipogenesis of preadipocytes via NADPH oxidase/ROS/p42/p44 MAPK-dependent COX-2 expression.

1 INTRODUCTION

Obesity is a world-wide problem, with the complication of various metabolic diseases. The problems of children with overweight and obesity are more and more serious, with over 41 million children under the age of 5 diagnosed with overweight or obese. It is found that obesity can be developed as early as child age between 2 and 6. The expansion of fat mass in child age includes both hyperplasia and hypertrophy of adipose tissue, suggesting the importance of proliferation and adipogenesis of preadipocytes.Though the hypertrophy of fat cells is reported as the characteristic of obese during the development, the hyperplasia of adipose tissue gains more and more notice. Because of the less expansion ability of fat cells, preadipocytes play the major roles in the increase of fat cell numbers.It is reported that the number of adipocytes is mostly stable through adulthood once determined in childhood and adolescence.However, recent studies in rodents have demonstrated that new adipocytes can originate from preadipocyte differentiation, which in turn can result in the expansion of adipose tissue during prolonged caloric excess.It is found that the hyperplasia of adipose tissue occurs in both genetic and diet-induced obese model and correlates with the disease severity and the poorest prognosis. Furthermore, there is an association between gut microbiota alteration and obesity development. The increase of Firmicutes and the decrease of Bacterioidetes and Bifidobacterium in obesity result in the decreased tight junction integrity and the increased gut permeability via the dysregulation of proglucagon-derived peptide (GLP)-2 expression. Lipopolysaccharide (LPS) is the major constituent that constitutes the cell wall of Gram-negative bacteria. Comparing to the levels in the blood, the concentration of LPS is much higher in the gut. Studies suggest that LPS enters the circulation via directly transcellular/paracellular transport through enteric barrier, or via the internalization and incorporation of chylomicrons. Once entering the circulation, LPS may exert its function as a pro-inflammatory regulator to promote the M1 phenotype changes of monocytes/macrophages. In addition, LPS may modulate and expand the adipose tissues. In fact, it has been found that Staphylococcus aureus infection leads to the expansion of human dermal fat layer.

Den gemensamma nämnaren är,som jag tolkar texten, att mikrobiotan hos dessa barn är påverkad/förändrad mot gängse dito för friska barn.

Mikrobiota : Är den samling av mikroorganismer – såsom bakterier, svampar och virus – som lever naturligt i mag- och tarmkanalen.Här finns runt 100 000 miljarder bakterier som tillsammans väger mellan 1,5-2 kilo. 

I denna mikrobiota hittade de förändringar i molekylen Lipopolysaccharide (LPS) som ingår i nåt som heter Gramnegativa bakterier.Dessa består av små celler som ingår naturligt i en människas mikrobiota.

Lipopolysaccharide (LPS) is the major component of the outer membrane of Gram-negative bacteria. Lipopolysaccharide is localized in the outer layer of the membrane and is, in noncapsulated strains, exposed on the cell surface.

 

Denna molekyl (LPS) har alltså utsatts för påverkan vilket leder till förändrad funktion som resulterar i sämre metabolism (försämrad ämnesomsättning,dvs kroppen förmår inte att bryta ner föda på ett naturligt sätt). Voilá

 

Mitt förslag till forskarna : hitta vad som påverkat denna molekyl (LPS) så har ni snart ett listat ut ett läkemedel som fixar detta. Lyckas ni med det kommer ni bota en stor mängd av världens (sjukligt) överviktiga barn.

Ett Nobelpris hägrar i så fall. 😎

Forskarna har använt HoloMonitor för att studera och räkna dessa celler.

Verifikation hittas under Material and Methods

2.7 Cell number counts

The cells were cultured in 6-cm dishes and underwent various experimental conditions. After that, the numbers of the cells were counted using HoloMonitor M4 (Phase Holographic Imaging PHI AB, Lund, Sweden) following manufacturer's instruction.

Studien är som föregående förpublicerad då den troligtvis anses hålla en hög vetenskaplig/kvalitativ nivå.

 

Min kommentar

Ännu ett nytt användningsområde för HoloMonitor kan noteras. Och detta var alltså den 4e forskningsrapporten bloggen berättat om enbart under denna vecka.Kan man dra några slutsatser av det tror ni?

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