Structural Brain Changes Associated With Overweight Thiab Obesity Part 1

Kev rog rog yog ib qho teeb meem kev noj qab haus huv thoob ntiaj teb nrog ntau cov kab mob sib txawv, xws li kev noj zaub mov tsis txaus, metabolic syndrome, ntshav qab zib, systemichypertension, plawv tsis ua haujlwm, thiab lub raum tsis ua haujlwm. /is tshuaj xyuas piav qhia txog kev tshawb pom tsis ntev los no ntawm neuroimaging thiab ob txoj kev tshawb fawb ntawm celldensity txog lub luag haujlwm ntawm overnutrition-induced hypothalamic o hauv neurodegeneration. /ese cov kev tshawb fawb tau muab cov pov thawj sib xws ntawm me me cortical thickness los yog txo cov teeb meem grey nyob rau hauv cov neeg uas rog dhau thiab rog; txawm li cas los xij, cov cheeb tsam hauv lub hlwb tau sib txawv ntawm cov kev tshawb fawb.

Systemic hypertension yog ib yam kab mob uas tshwm sim los ntawm kev nce ntshav siab mus ntev, uas ua rau muaj kev puas tsuaj loj rau tib neeg kev noj qab haus huv. Kev nco yog ib qho tseem ceeb thiab tseem ceeb ua haujlwm hauv tib neeg lub neej txhua hnub. Nws ua lub luag haujlwm tseem ceeb hauv kev ua haujlwm, kev kawm, lub neej, thiab lwm yam. Yog li, dab tsi yog kev sib raug zoo ntawm kev kub siab thiab kev nco?

Kev tshawb fawb qhia tau hais tias muaj tseeb muaj kev sib raug zoo ntawm lub cev kub siab thiab nco. Ntshav siab tuaj yeem cuam tshuam ncaj qha rau tib neeg lub hlwb kev noj qab haus huv. Cov ntshav tsis txaus rau lub hlwb tshwm sim los ntawm cov ntshav siab ntev yuav ua rau muaj kev puas tsuaj ncaj qha rau cov neurons thiab vascular hlwb hauv lub hlwb. Tsis tas li ntawd, ntshav siab feem ntau nrog ntau yam mob xws li hyperlipidemia, kab mob plawv, mob stroke, thiab ntshav qab zib. Cov xwm txheej no tseem yuav ua rau muaj kev cuam tshuam ntawm cov ntshav siab ntawm lub hlwb. Cov xwm txheej no yuav cuam tshuam ncaj qha lossis tsis ncaj rau tib neeg txoj kev loj hlob thiab kev xav muaj peev xwm, thiab inhibit qhov kev loj hlob ntawm kev nco.

Txawm li cas los xij, tsis txhob ua pessimistic dhau lawm. Qhov tseeb, rau feem ntau cov neeg mob ntshav siab, tsuav yog lawv siv sijhawm sijhawm thiab ntsuas tau zoo, ua haujlwm kho thiab tshawb fawb tswj ntshav siab, nws muaj peev xwm tiv thaiv lub hlwb ua haujlwm. Ntau yam kev hloov kho lub neej, xws li kev noj zaub mov kom tsim nyog, kev tawm dag zog tsim nyog, txo kev ntxhov siab, thiab ua kom tsaug zog txaus, yog txoj hauv kev zoo heev los tiv thaiv thiab kho ntshav siab. Tsis tas li ntawd, cov tshuaj antihypertensive uas tus kws kho mob tau sau tseg kuj yuav tsum tau noj raws li tus kws kho mob cov lus qhia, thiab cov tshuaj yuav tsum tsis txhob hloov lossis nres ntawm qhov xav tau.

Nyob rau hauv luv luv, kev sib raug zoo ntawm systemic hypertension thiab nco yog muaj feem xyuam rau ib tug npaum li cas, tab sis nws tsis tau txhais hais tias kub siab yog tus culprit ntawm nco poob. Tsuav yog peb siv cov kev kho mob zoo thiab tswj cov ntshav siab raws li kev tshawb fawb thiab kev xav, lub hlwb noj qab haus huv thiab kev nco ntse yuav dhau los ua qhov tseem ceeb hauv peb lub neej thiab kev ua haujlwm. Nws tuaj yeem pom tias peb yuav tsum txhim kho kev nco, thiab Cistanche deserticola tuaj yeem txhim kho kev nco zoo vim Cistanche deserticola yog cov khoom siv tshuaj hauv Suav teb uas muaj ntau yam teebmeem, ib qho ntawm kev txhim kho kev nco. Kev ua tau zoo ntawm Cistanche deserticola los ntawm ntau yam khoom xyaw uas nws muaj, suav nrog tannic acid, polysaccharides, flavonoid glycosides, thiab lwm yam. Cov khoom xyaw no tuaj yeem txhawb lub hlwb kev noj qab haus huv los ntawm ntau txoj hauv kev.

Nyem paub 10 txoj hauv kev los txhim kho kev nco

Feem ntau, ob sab pem hauv ntej thiab sab cev nqaij daim tawv, basal nuclei, andcerebellum feem ntau koom nrog. Mechanisms ntawm kev txo ntim tsis paub, thiab neuroinflamation los ntawm kev rog dhau yuav ua rau muaj kev puas hlwb neuronal.

Adipocytes, macrophages ntawm cov ntaub so ntswg adipose, thiab plab dysbiosis nyob rau hauv rog rog thiab obeseindividuals ua rau lub secretion ntawm cytokines thiab chemokines uas hla cov ntshav-hlwb barrier thiab tej zaum yuav tsub kom microglia, uas nyob rau hauv lem kuj tso tawm proinflammatory cytokines. / yog ua rau mob qis-qib neuroinflammation thiab tej zaum yuav yog qhov tseem ceeb rau apoptotic signaling thiab neuronal tuag.

Tsis tas li ntawd, qhov tseem ceeb ntawm microangiopathy tau pom hauv cov qauv nas yuav yog lwm qhov tseem ceeb ntawm kev cuam tshuam ntawm apoptosis. Neuroinflammation nyob rau hauv cov kab mob neurodegenerative (xws li Alzheimer's thiab Parkinson's kab mob) tej zaum yuav zoo ib yam li cov kab mob metabolic tshwm sim los ntawm kev noj tsis txaus.

Kev paub txog kev ua haujlwm tsis zoo, feem ntau hauv kev tswj hwm kev ua haujlwm, hauv cov neeg muaj rog kuj tau tham txog. /is tshuaj xyuas qhia txog cov neuroinflammatory thiab neurodegenerative mechanisms txuas rau kev rog rog thiab hais txog qhov tseem ceeb ntawm kev txhim kho kev tiv thaiv zoo thiab kev kho mob cov tswv yim rau cov neeg rog rog thiab rog.

1. Taw qhia

Kev rog rog yog ib qho teeb meem loj thoob ntiaj teb uas cuam tshuam nrog kev noj qab haus huv, lub cev nqaij daim tawv, kev coj cwj pwm, kev sib raug zoo, ib puag ncig, kev lag luam, thiab kev nom kev tswv [1]. Kev sib kis ntawm kev rog rog tau mus txog thaum kawg ntawm lub xyoo pua txij li kev rog dhau los ua ib qho ua rau tuag, kev tsis taus thoob ntiaj teb [2], thiab lub nra nyiaj txiag tseem ceeb [3].

Nyob rau xyoo 1970, pawg kws tshaj lij los ntawm United Kingdom thiab Tebchaws Meskas tau hais txog qhov yuav tsum tau xav txog qhov tshwm sim tshiab ntawm kev rog rog uas yog ib qho tseem ceeb, uas thaum lub sijhawm ntawd tsuas yog cuam tshuam rau cov neeg laus, tshwj xeeb yog cov poj niam [4]. Tsis tas li ntawd, kev rog rog yog qhov hnyav dua los ntawm qhov tsis muaj kev xaiv kho mob zoo [5].Hauv xyoo 2016, ntau dua 1.9 billion tus neeg laus hnub nyoog 18 xyoo thiab laus dua rog, ntawm ntau dua 650 lab tus neeg muaj rog. / cov lej no suav nrog 39% ntawm cov neeg laus dua 18 xyoo (39% txiv neej thiab 40% poj niam), uas rog dhau, thiab 13% ntawm cov neeg laus hauv ntiaj teb (11% txiv neej thiab 15% poj niam) tsim rog [6].

Hauv plaub lub xyoos dhau los, qhov ntau ntawm kev rog rog tau ze li peb npaug thoob ntiaj teb. Ntau tshaj 340 lab tus menyuam yaus thiab cov tub ntxhais hluas hnub nyoog txij li tsib xyoos txog rau kaum cuaj xyoo tau hnyav dhau los lossis rog dhau xyoo 2016, thiab kwv yees li 38.2 lab tus menyuam yaus hnub nyoog qis dua tsib xyoos tau rog lossis rog hauv 2019 [6]. Yog tias tsis ntev los no txuas ntxiv mus, nws kwv yees tias, los ntawm 2030, 60% ntawm cov pej xeem hauv ntiaj teb (3.3 billion tus neeg) yuav rog dhau (2.2 billion) lossis rog (1.1 billion) [7].

Kev rog dhau thiab rog tau txuas nrog ntau tus neeg tuag thoob ntiaj teb tshaj qhov hnyav dua, nrog kev rog dhau 50% hauv ntau lub tebchaws [8].Lub cev qhov hnyav (BMI) yog ib qho kev siv dav tshaj plaws los txheeb xyuas qhov hnyav hnyav txog qhov siab thiab hnub nyoog. /e Lub Koom Haum Saib Xyuas Kev Noj Qab Haus Huv (World Health Organization) categorizes obesityin cov ntsiab lus ntawm BMI: qis dua (BMI tsawg dua 18.5 kg / m2), qhov hnyav li qub (ntau txog 18.5 txog 25 kg / m2), rog dhau (ntau txog 26 txog 30 kg / m2), thiab rog ( ntau dua 30 kg / m2) [6, 9].

Txawm li cas los xij, kev siv BMI ua qhov ntsuas ntawm qhov hnyav lossis rog tsis tuaj yeem ntseeg tau rau txhua tus neeg; BMI tau siv rau hauv cov neeg laus, txawm hais tias tam sim no tau siv cov menyuam yaus thiab cov neeg laus. Hauv cov menyuam yaus thiab cov tub ntxhais hluas, BMI z-cov qhab nia raug siv vim tias, hauv cov pejxeem no, BMI txawv nrog lub hnub nyoog thiab poj niam txiv neej [10] (BMI z-tus qhab nia yog txhais tau tias yog qhov ntsuas ntawm tus txheeb ze qhov hnyav hloov kho rau cov menyuam hnub nyoog thiab poj niam txiv neej txog cov neeg siv) ./e duav-rau-hip piv (WHR) yog lwm qhov kev siv dav dav uas ntsuas qhov kev faib tawm ntawm cov ntaub so ntswg adipose [11].

Lub cev rog hauv nruab nrab yog txuam nrog kev nce ntxiv ntawm cov ntaub so ntswg hauv plab adipose, txawm hais tias qhov nce insubcutaneous plab plab adipose cov ntaub so ntswg kuj koom nrog.Txawm li cas los xij, WHR tsis yog qhov ntsuas tsis zoo vim lub plab ncig ib leeg tuaj yeem muab cov ntaub ntawv tib yam [11] .Dual-zog X-ray absorptiometry (DXA) yog ib qho kev siv ntau hauv tsev kho mob los ntsuas lub cev muaj pes tsawg leeg (pob txha pob txha, rog, lean, thiab cov nqaij mos) siv cov xoo hluav taws xob xoo hluav taws xob tsawg. DXA muab cov ntaub ntawv hais txog adiposity ntau dhau thiab suav cov rog tag nrho thiab cov nqaij mos ntshiv [12].

Kev hloov pauv huab cua plethysmography (ADP) yog lwm txoj hauv kev los ntsuas lub cev muaj pes tsawg leeg (bonedensity, lean ntaub so ntswg, thiab tag nrho lub cev rog). ADP kwv yees lub cev ntim ntawm ib tug neeg los ntawm kev xam qhov ntim ntawm cov huab cua nyob rau hauv ib lub chamber npliag rho tawm qhov ntim ntawm cov huab cua nrog ib tug neeg zaum nyob rau hauv lub chamber [13].

Skinfolds yog ib txoj kev siv anthropometric uas siv los ntsuas cov roj subcutaneous, txawm hais tias lawv tsis pom zoo rau qee cov neeg laus uas rog dhau thiab rog. Ntxiv mus, standardized skinfold caliper ntsuas arelacking; yog li ntawd, tsis muaj kev pom zoo hais txog qhov kev faib tawm ntawm cov rog subcutaneous ntsuas hauv cov pejxeem [11].

2. Pathogenesis ntawm Obesity

Kev rog rog tshwm sim los ntawm qhov tsis muaj qhov sib npaug ntawm kev noj zaub mov thiab kev siv zog [14]. Kev siv hluav taws xob suav nrog lub zog xav tau los tswj kev ua haujlwm tseem ceeb (so metabolic rate), ua lub cev ua si, thiab muab cov khoom noj uas muaj thermogenesis.

Cov kev tshawb fawb luam tawm tsis tau txhawb nqa qhov kev xav tias kev rog yog tshwm sim los ntawm kev cuam tshuam ntawm kev siv hluav taws xob cuam tshuam nrog cov metabolism thiab / lossis kev noj zaub mov-vim thermogenesis; Hloov chaw, pov thawj qhia tias kev ua kom lub cev poob qis tuaj yeem ua rau lub cev hnyav nce [15] ./e kev siv hluav taws xob xav tau los tswj qhov hnyav sib txawv ntawm cov tib neeg, suav nrog cov tib neeg nrog cov kev cai sib xws. Qhov sib txawv hauv kev ua haujlwm hauv metabolic tuaj yeem piav qhia qhov hloov pauv no thiab ua lub luag haujlwm hauv qhov hnyav nce [15].

Kev hloov pauv ntawm lipids thiab carbohydrates rau hauv kev ua haujlwm tiag tiag yuav tsum tau oxidation ntawm cov as-ham kom tawm los adenosine triphosphate (ATP), uas ua haujlwm raws li cov txiaj ntsig metabolic [15], thiab ATP yog tom qab siv los ua cov haujlwm tiag tiag (xws li, lub cev tseem ceeb thiab kev ua haujlwm ntawm lub cev) [15] ]. Ob qho ntawm cov txheej txheem metabolic no suav nrog kev tsim hluav taws xob. / peb, metabolic efficiency yog hais txog qhov kev faib ua feem ntawm ATP piv rau kev tsim cov cua sov los ntawm kev ua haujlwm ntawm ib txoj haujlwm [16]. /e muaj peev xwm pov tseg ntawm ib feem ntawm lub zog ntau dhau vim qhov cua sov txo lub peev xwm khaws cov roj ntau dhau thiab yog li tiv thaiv qhov hnyav nce [16]. Lowmetabolic efficiency txhais tau hais tias qhov nce hauv cov khoom cua sov ntawm cov nqi ntawm ATP ntau lawm [16].

Txhim kho metabolicefficiency tau raug tshaj tawm los txhawb kev rog [16] ./e sympathetic nervous system (SNS) koom nrog inhomeostatic tswj. Kev yoo mov txo SNS kev ua si thaum noj, tshwj xeeb tshaj yog carbohydrate overfeeding, nce SNSactivity. /e SNS innervates thiab modulates lipolysis hauv cov ntaub so ntswg adipose [17]. Parasympathetic cov tswv yim tuaj yeem kho qhov theetiology ntawm kev rog los ntawm kev cuam tshuam ncaj qha rau lub xeev metabolic ntawm cov ntaub so ntswg adipose.

Neuroimmune kev sib cuam tshuam ntawm SNS thiab macrophages yog xav tau rau homeostasis ntawm ntau cov ntaub so ntswg, nrog rau cov ntaub so ntswg adipose [18]. / peb, SNS-mediated txo nyob rau hauv cov nqaijrog lipolysis pab txhawb tolipid tsub zuj zuj thiab, yog li ntawd, ntau tshaj qhov hnyav [17] ./e lub hlwb thiab plab hnyuv ib ntsuj av tau txuas ntawm lub paj hlwb. Intra-abdominal adipocytes txhawb nqa cov piam thaj thiab fatty acid kom tsawg los ntawm kev txhawb nqa SNS; cov cellexpress adrenergic receptors uas muaj peev xwm teb rau catecholamines ntawm lub sympathetic system. /e cholinergic ib feem ntawm cov hlab ntsha vagus koom nrog kev tswj hwm ntawm cov piam thaj thiab insulin [17].

Acetylcholine ua los ntawm cov hlab ntsha vagus topotentiate M3 muscarinic receptors ntawm pancreas kom nce insulin secretion, txhim kho cov synthesis ntawm cellularlipids thiab nqus cov piam thaj, uas ua rau khaws cov calories thiab nce lipids [17]. / Lub paj hlwb enteric tsim ntau tshaj 30 neurotransmitters; Cov tshuaj hormones thiab peptides raug tso tawm rau hauv cov hlab ntsha, hla cov hlab ntsha hlwb (BBB), thiab txhawb nqa lub hauv paus paj hlwb (CNS). Thaum noj tshuaj, cov tshuaj hauv plab hnyuv tau tso tawm vim qhov mob plab, xws li thepeptides cholecystokinin, ghrelin, thiab leptin, uas tswj cov kev xav ntawm kev tshaib kev nqhis thiab satiety. Ghrelin txhawb kev noj zaub mov los ntawm inhibiting lub vagal signals thiab inhibiting qhov tso tawm ntawm insulin [17].

Leptin thiab insulin koom nrog cov teebmeem no ntawm SNSactivity. Leptin yog ib qho adipocyte-tsim cov tshuaj hormones uas tau tswj hwm hauv kev rog [19]. Leptin teeb liab nyob rau hauv lub hlwb loj ntawm qib ntawm hypothalamus los hloov cov kev ua haujlwm ntawm cov neuronal subsets (xws li orexigenicAgouti-related peptide (AgRP) thiab anorexigenic proopiomelanocortin (POMC) neurons), txo qab los noj mov, thiab nce zog siv [20].
Leptin ua haujlwm raws li ib qho kev taw qhia kom ncig lub zog tshwj xeeb los ntawm kev muab cov lus tawm tswv yim inhibition hauv txoj kev hypothalamic orexigenic; Yog li, kev rog rog yog txuam nrog hyperleptinemia [5]. Kev rog rog yog tus cwj pwm los ntawm kev tsis pom zoo leptin taw qhia txawm tias nce qib leptin, uas yog, leptin tsis kam, uas piav qhia vim li cas leptin kev tswj hwm rau feem ntau cov neeg rog rog yog qhov tseem ceeb [20].

Leptin kuj ntseeg tau tias yog qhov tshwm sim ntawm kev mob plab thiab hypothalamic gliosis [20–22]. Kev noj zaub mov kom ntev ntev rau cov nas ua rau cov nas ua kom mediobasal hypothalamic ua kom cov kab mob inflammatory intermediates c-Jun N-terminal kinase (Jnk) thiab nuclear factorκB (NF-κB), uas ua rau kev tsim cov cytokines proinflammatory thiab tsis zoo nyob rau hauv. insulin thiab leptinsignal [22]

Tsis tas li ntawd, cov lus teb ntawm tes rau kev noj zaub mov muaj roj ntau hauv hypothalamus suav nrog reactive gliosis [18], uas yog CNS cov txheej txheem tshwj xeeb ntawm kev nrhiav neeg ua haujlwm, kev loj hlob, thiab kev hloov pauv morphological ntawm astrocytes thiab microglia cuam tshuam rau lub hlwb raug mob. /is cellular teb alters neurovascular coupling ntawm POMC neurons vim ensheathment ntawm cov synapses los hloov cov neurotransmitter dynamics byaltering astrocyte qhia ntawm glutamate thiab glucosetransporters hloov cov firing kev ua ntawm POMC neurons [22].

Cov txheej txheem nyuaj uas tswj hwm tus cwj pwm noj mov sib npaug ntawm kev sib raug zoo ntawm kev noj haus (kev noj haus) thiab kev siv hluav taws xob. /ese systems muaj kev cuam tshuam rau kev cuam tshuam los ntawm lub zog tsis txaus. /e hedonic thiab homeostatic txoj kev tswj kev noj zaub mov. /e hedonicsystem tso siab rau ntawm striatum thiab muaj kev sib txuas ze rau lub hypothalamus thiab homeostatic system [23].

Ib qho khoom plig tsis txaus yog suav tias ua rau muaj qhov tsis sib xws ntawm kev tswj hwm homeostatic thiab hedonic. /is hypothesis qhia tias txo qis dopaminergic signaling, uas feem ntau xa cov txiaj ntsig zoo ntawm (khoom noj khoom haus) stimuli, txhawb kev noj ntau dhau ntawm cov khoom noj qab tshaj li qhov xav tau ntawm homeostatic los them rau qis dua rau qhov khoom plig [24].

Txo serotonin signaling nyob rau hauv lub hypothalamus yog assumed los pab rau kev rog los ntawm kev cuam tshuam negativefeedback ntawm lub zog noj ntawm cov zaub mov noj, yog li txhawb kev noj ntau heev [25] ./e paraventricular nucleus ntawm lub hypothalamus tsim peptides uas txo nrog zaub mov noj, nrog rau thyrotropin-tso tshuaj hormones, -releasingfactor, thiab oxytocin. Cannabinoids tswj kev qab los noj mov, thiab cov kab mob cytokines tseem koom nrog kev tswj hwm ntawm lub plab zom mov paj hlwb [19].

Inflammation nyob rau hauv lub hypothalamus tuaj yeem ua rau muaj kev sib txawv ntawm tus cwj pwm. / peb, qhov nce siab hauv cov qib hypothalamic cytokine tau pom nyob rau hauv qhov sib sib zog nqus-anorexia animalmodels, ob qho tib si nyob thiab ntawm nws tus kheej ntawm leptin [5] .Hypothalamic tsis kam rau cov teebmeem ntawm leptin ntawm cov ntaub so ntswg adipose yog qhov tseem ceeb rau kev rog rog. Hypothalamic o yog tshwm sim los ntawm kev teb rau kev noj cov roj ntau ntau txhua hnub thiab yog ib qho tseem ceeb hauv kev txhim kho leptin tsis kam [26].de Araujo li al. [27] suav tias yog cov teebmeem tseem ceeb ntawm lub zog cov ntsiab lus ntawm cov zaub mov kho los ntawm plab-innervatingsensory vagal neurons (lub plab-hlwb axis txoj hauv kev) uas ua raws li ib daim ntawv ntawm ib qho khoom plig interoceptive, uas yog ywj siab ntawm palatability.

Cov tib neeg uas muaj rog rog tsis qhia txog kev nyiam noj zaub mov ntau dua li lawv cov khoom noj qab haus huv. Palatability cuam tshuam rau tus neeg noj dab tsi tab sis tsis cuam tshuam qhov tus neeg no noj ntau npaum li cas. /e cov ntsiab lus ntawm cov zaub mov muaj zog ntxiv. Raws li de Araujo et al. /e kev txhawb zog ntawm lub zog ntom ntom pom muaj zog rau cov neeg rog rog.

Txawm li cas los xij, lub plab microbiota tau xav tias ua lub luag haujlwm hauv cov txheej txheem tswj hwm kev ntxhov siab los ntawm hypothalamic pituitary adrenal (HPA) axis, thiab deregulation ntawm cov axis no kuj tau cuam tshuam txog kev rog [28]. / e gutbrain axis yog ib txoj hauv kev uas ua rau kev sib txuas lus nruab nrab ntawm lub plab thiab lub hlwb los ntawm hormonal, immunological, thiab neural signals. /e CNS, autonomous nervoussystem, enteric nervous system, HPA axis, thiab plab microbiota yog cov khoom ntawm lub plab-hlwb axis.

Tag nrho cov khoom sib txuas no tsim kev sib txuas lus los ntawm CNS mus rau lub plab thiab los ntawm lub plab mus rau CNS [29].

Lub plab cov tshuaj hormones raug tso tawm los ntawm cov hlwb enteroendocrine uas ua rau muaj teeb meem hauv CNS hauv cov lus teb rau cov khoom noj preabsorptive thiab tom qab ntawd cuam tshuam lub zog homeostasis [29].Raws li ib feem ntawm lub plab-hlwb hlwb, lub plab microbiota (cov kab mob uas nyob hauv tib neeg lub plab zom mov) ua si tseem ceeb. Lub luag haujlwm hauv adiposity thiab qhov hnyav nce los ntawm kev sau qoob loo, tiam tom qab ntawm ntau yam metabolites (piv txwv li, luv-chain fatty acids), kev hloov pauv hauv tus cwj pwm, thiab satietythrough ntawm lub plab-hlwb axis uas induces inflammatory teb [29].

Kev rog rog, kab mob metabolic, qee qhov kev puas siab puas ntsws, thiab kev paub tsis meej tuaj yeem tshwm sim los ntawm kev ua haujlwm tsis zoo ntawm cov kab ke no [28, 29]./Muaj kev sib raug zoo ntawm kev ntxhov siab (cov qib siab ntawm glucocorticoids), qhov hnyav nce, adiposity, BMI [30], basal qabzib, basal insulin, thiab insulin tsis kam [31].Kev sib koom ua ke ntawm kev ntxhov siab nrog kev ua haujlwm tsis zoo ntawm cov metabolism hauv cov tib neeg muaj BMI siab dua li cov neeg uas muaj BMI qis dua [32], qhia tias kev ntxhov siab ua rau muaj kev rog rog, tshwj xeeb tshaj yog rau cov neeg uas muaj BMI siab dua.

Cov qib siab ntev ntawm glucocorticoids thiab insulin boost ib qho kev nce hauv cov zaub mov tsis txaus noj thiab cov rog hauv plab [33].Kev ntxhov siab tuaj yeem ua rau cov metabolism tsis ua haujlwm thiab hloov pauv kev noj zaub mov; Tsis tas li ntawd, cov tib neeg uas muaj rog rog ntau dua rau kev ntxhov siab. /e HPA axis plays lub luag haujlwm tseem ceeb hauv qhov pib ntawm kev hloov pauv hauv metabolic thiab rog [34].

3. Kev rog rog thiab Neuroinflamation

Macrophages tswj kev mob raws li ntau lub xeev kev ua haujlwm nyob ntawm lawv lub xeev ntawm kev sib txawv; yog li, classical activated macrophages (M1) pib txheej txheem los ntawm secreting proinflammatory cytokines thiab reactive oxygen hom (ROS) [35], whereas tom qab theem ntawm lub cev tiv thaiv kab mob yog tswj los ntawm "lwm yam. " activated macrophages (M2) kom txo tau qhov mob thiab txhawb cov ntaub so ntswg hloov kho thiab tso tawm ntawm qhov kev loj hlob [35].

Hauv cov tib neeg noj qab haus huv, tsis muaj neeg noj qab haus huv, macrophages hauv cov ntaub so ntswg adipose ua haujlwm zoo ib yam li M2 macrophages; uas yog, lawv tsim me ntsis kom tsis muaj proinflammatory cytokines thiab nthuav qhia arginase, uas inhibits nitric oxide ntau lawm thiab ua rau polyamine tiam [36]. Txawm li cas los xij, adipose cov ntaub so ntswg txuam nrog macrophages nyob ntawm qhov chaw ntawm chronicinflammation hauv kev rog tuaj yeem ua raws li qhov chaw ntawm proinflammatory cytokines [37].

Ob leeg M1 thiab M2 macrophages tuaj yeem sib koom ua ke, ua rau muaj mob tsis tu ncua thiab fibrosis [38] .Kev sib sau ntawm cov ntaub so ntswg adipose hauv kev rog yog qhov tseem ceeb ntawm kev mob plab. Ob leeg hypertrophic adipocytes thiab lub cev tiv thaiv kab mob nyob hauv cov ntaub so ntswg adipose (feem ntau yog lymphocytes thiab macrophages) ua rau apro-inflammatory xeev los ntawm kev nce qib ntawm cov qog nqaij hlav-alpha (TNF-), plasminogen activator inhibitor -1, C- reactive protein, interleukin-1-beta (IL-1-beta), thiab interleukin{10}} (IL-6) [39, 40]. /e inflammatory responsemediated los ntawm M1 thaum rog rog tej zaum yuav zoo ib yam rau cov txheej txheem ntawm necrotic clearance [41, 42].

Macrophagessecrete cytokines, tshwj xeeb tshaj yog TNF thiab IL-6, thiab chemokines, xws li CC-chemokine ligand 2 (CCL2; yav tas los hu ua asmonocyte chemotactic protein-1 (MCP1)). TNF thiab IL-6 tuaj yeem cuam tshuam nrog cov teeb liab insulin hauv adipocytes, ua rau mob ntshav qab zib hom 2 (T2DM) [43]. Macrophages khaws cov ntaub so ntswg inadipose dhau sijhawm, thiab cov cytokines uas lawv tsim tuaj yeem ua rau insulin tsis kam thiab T2DM [36, 37].

Overexpression ntawm procoagulant proteins los ntawm cov kab mob inflammatory macrophages tuaj yeem ua rau muaj kev pheej hmoo ntawm atherogenic thiab plawv plawv uas yog ib feem ntawm kev rog rog-associatedmetabolic syndrome [43].Txawm li cas los xij, kev rog rog cuam tshuam nrog plab hnyuv microbiota kuj tseem tuaj yeem ua rau muaj kev cuam tshuam rau neurochemical thiab inflammatory alterations [28.4] /e plab microbiota yog qhov nruab nrab ntawm ib puag ncig kev nyuaj siab (xws li, kev noj haus thiab kev ua neej) thiab tus tswv lub cev, thiab nws qhov kev hloov pauv (xws li, dysbiosis) tuaj yeem piav qhia txog kev rog [28].

Lub plab dysbiosis (kev tsis txaus ntseeg hauv gutmicrobiota muaj pes tsawg leeg tshwm sim los ntawm cov noob caj noob ces, kev ua neej, thiab raug cov kab mob) [45] tuaj yeem txhawb kev noj zaub mov vim kev rog thiab cov teeb meem metabolic los ntawm ntau yam txheej txheem, suav nrog kev tiv thaiv kab mob, hloov pauv lub zog, kev hloov pauv hauv plab, thiab cov tshuaj hormones. mechanisms (xws li lipopolysaccharideendotoxins uas hla lub plab barrier thiab nkag mus rau portalcirculation) [44, 46].

Cov kev tshawb fawb tsis ntev los no tau pom tias muaj kev hloov pauv hauv lub plab thiab qhov mob ntsig txog lub plab hnyuv (qhov poob ntawm cov plab hnyuv siab rau kev ua kom tsis muaj peev xwm los tiv thaiv ib puag ncig sab hauv) tuaj yeem ua rau cov kab mob pathophysiology ntawm ntau yam kab mob, xws li kev nyuaj siab, mob nkees nkees, rog, lossis T2DM [ 47].Cov kab mob uas tshwm sim los ntawm kev rog tuaj yeem cuam tshuam rau lub hlwb, xws li hippocampus, cerebral cortex, brainstem, thiab amygdala [48].

Qib qis tus yam ntxwv ntawm kev rog rog tuaj yeem ua rau neuroinflammation viav vias mechanisms, suav nrog choroid plexuses thiab cuam tshuam ntawm BBB [49]. Cov kab mob peripheral pom hauv kev rog rog ua rau insulin tsis kam [36, 37]. / Thebrain yog lub cev muaj cai rau kev tiv thaiv kab mob; Txawm li cas los xij, kev hloov pauv ntawm peripheral thiab central o tau raug tshaj tawm.

Adipokines yog tsim los ntawm adiposetissue thiab tuaj yeem hais tawm hauv CNS, qhov twg receptors rau cov xwm txheej no. Adipokines tsim nyob rau hauv lub periphery tuaj yeem hla BBB lossis hloov kho nws lub cev los ntawm kev ua haujlwm ntawm cov hlwb uas tsim BBB los cuam tshuam rau CNS.

Adipokines tuaj yeem tswj hwm neuroinflammation thiab oxidativestress, uas yog ob qho tseem ceeb physiological txheej txheem koom nrog hauv neurodegeneration thiab cuam tshuam nrog ntau yam kab mob neurodegenerative [50]. Kev puas tsuaj rau BBBin kev laus kuj tuaj yeem ua rau mob hauv lub hlwb. Neuroinflammation tej zaum yuav yog qhov tseem ceeb tshaj plaws ua rau lub hlwb tsis ua haujlwm thiab tuaj yeem ua rau lub hauv paus pathological txheej txheem cuam tshuam nrog kev laus [51].

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