A belekben élő mikrofl óra -bélbakterióta -évtizedek óta ismert, de egyre újabb funkcióit megismerve ismét a tudományos érdeklődés középpontjába került. A bélrendszerben 100 000 billió baktérium él. A bélbakterióta a bélrend-szer különböző szakaszaiban változó összetételben és mennyiségben helyezkedik el, életkortól, testsúlytól, földrajzi elterjedéstől, étrendtől függően. A normális bélfl óra megvédi a szervezetet a káros mikroorganizmusok behatolásá-tól, elősegíti az emészthetetlen rostok emészthetővé tételét, biztosítja a bélnyálkahártya integritását, befolyásolja a szervezet immunitását, inzulinérzékenységét, a testsúlyt, sőt az agy működésével is kölcsönhatásban van. A bélbakte-rióta hatására a vastagbélben szénhidrátok fermentációjából rövid láncú zsírsavak -butirátok, acetátok, propionátok -keletkeznek, amelyek kedvezően hatnak a metabolikus folyamatokra. Új észlelés az agy-bél tengely létezése, a mikrobióta közvetlenül hat az agyi központokra, ahonnan információk érik a mikrobiótát. E kétirányú folyamatban részt vesz az immun-és neuroendokrin rendszer, az autonóm és a centrális idegrendszer is. A bélmikrobióta műkö-dése függ a cirkadián ritmus változásától is. A gazdaszervezet és a bélfl óra közötti egyensúly megbomlása dysbacteriosist okoz, Gram-negatív baktériumok által termelt endotoxinok (lipopoliszacharidok) jutnak a keringésbe (metabolikus endotoxaemia) a bélnyálkahártya permeabilitásának fokozódása útján, amelyek immunreakciót és gyulladást indukálnak. Ezek a folyamatok elhízást, inzulinrezisztenciát, diabetest, metabolikus szindrómát, gyulladásos bélbe-tegséget, autoimmunitást, daganatképződést okozhatnak. Biztató terápiás lehetőség e betegségek gyógyításában az egészséges bélfl óra helyreállítása probiotikumok, prebiotikumok útján. Egészséges egyénből származó széklet transzplantációja az elhízott egyén minden kóros metabolikus paraméterét javította. Remélhető, hogy a mikrobióta alaposabb megismerése hatásos gyógymódok kifejlesztését fogja eredményezni. Orv. Hetil., 2016, 157(1), 13-22.Kulcsszavak: mikrobióta, dysbiosis, metabolikus endotoxaemia, rövid láncú zsírsavak (SCFA-k), agy-bél tengely, fekális transzplantáció, bariátrikus sebészet Physiological patterns of intestinal microbiota. The role of dysbacteriosis in obesity, insulin resistance, diabetes and metabolic syndromeThe intestinal microbiota is well-known for a long time, but due to newly recognized functions, clinician's attention has turned to it again in the last decade. About 100 000 billion bacteria are present in the human intestines. The composition of bacteriota living in diverse parts of the intestinal tract is variable according to age, body weight, geological site, and diet as well. Normal bacteriota defend the organism against the penetration of harmful microorganisms, and has many other functions in the gut wall integrity, innate immunity, insulin sensitivity, metabolism, and it is in cross-talk with the brain functions as well. Brand new recognition, that intestinal microbiota has a direct effect on the brain, and the bra...
The existence of insulin-like growth factors (IGFs) was recognized in connection with the stimulation of sulfate incorporation into cartilage. IGFs take part in the embryonal development and postnatal growth, in interaction with the growth hormone (GH). The physiological effects of IGF1 are promotion of tissue growth and development, stimulation of cell proliferation, effects on lipid and carbohydrate metabolism, anti-aging, anti-inflammatory, anabolic, anti-oxidant, neuro- and hepatoprotective properties. Our knowledge about the GH/IGF axis is diverse, partly contradictory, their research is continued intensively nowadays. We considered it worthwhile to review and interpret this information. Study on GH/IGF medical reports, with particular reference to the less known metabolic control. 75% of the growth factors are produced in the liver by GH and insulin stimulation; their effects are expressed on specific receptors, and modified by specific binding proteins. IGF1 directly increases the muscle mass, bone density, and the structure of the bones. Intestinal microbiota induces secretion of IGF1, which promotes the development and remodeling of the bones. Short-chain fatty acids, produced in microbial fermented fibers, induce secretion of IGF1, suggesting that microbial activity also affects bone health via IGF1. IGF1 also has a direct and indirect glucose-lowering effect, enhances free fatty acid oxidation in the muscle, reducing the flow of free fatty acid into the liver, improving insulin signaling, resulting in the reduction of hepatic glucose output, and improves insulin sensitivity. IGF1 directly influences the expression of circadian BMAL1 in hypothalamic cells: this refers to the newly recognized ’zeitgeber’ role of IGF1. The bioactivity of insulin-like peptides in the brain is characterized by neuronal survival, excitatory and inhibitory neurotransmission, maintenance of normal free fatty acid levels, improvement of cognitive function, protection against cell damage, neurogenesis and angiogenesis. The effects of IGF2 are less outlined, however, it has a relevant role in the development of the fetus, and acts protectively on the brain. Lack or over-expression of IGF1 can be detected or may causally associated in many pathological conditions. According to these collected data, insulin sensitivity may be improved by different pathways. The role of IGFs in these processes should be a task of future research. Orv Hetil. 2019; 160(45): 1774–1783.
Non-alcoholic fatty liver disease is the most common non-infectious chronic liver-disease in our age, and is a spectrum of all the diseases associated with increased fat accumulation in the hepatocytes. Its development is promoted by sedentary life-style, over-feeding, and certain genetic predisposition. Prevalence in the adult population, even in Hungary is ~30%. In a part of cases, this disease may pass into non-alcoholic steatohepatitis, later into fibrosis, rarely into primary hepatocellular cancer. Fatty liver is closely and bidirectionally related to the metabolic syndrome and type 2 diabetes, and nowadays there is a general consensus that fatty liver is the hepatic manifestation of the metabolic sycndrome. The importance of the fatty liver has been highly emphasized recently. In addition to the progression into steatohepatitis, its causal relationship with numerous extrahepatic disorders has been discovered. In our overview, we deal with the epidemiology, pathomechanism of the disease, discuss the possibilities of diagnosis, its relationship with the intestinal microbiota, its recently recognized correlations with bile acids and their receptors, and its supposed correlations with the circadian CLOCK system. Hereinafter, we overview those extrahepatic disorders, which have been shown to be causal link with the non-alcoholic fatty liver disease. Among these, we emphasize the metabolic syndrome/type 2 diabetes, cardiovascular disorders, chronic kidney disease, sleep apnea/hypoventilation syndrome, inflammatory bowel disease, Alzheimer's disease, osteoporosis, and psoriasis, as well. Based on the above, it can be stated, that high risk individuals with non-alcoholic fatty liver disease need systemic care, and require the detection of other components of this systemic pathological condition. While currently specific therapy for the disease is not yet known, life-style changes, adequate use of available medicines can prevent disease progression. Promising research is under way, including drugs, manipulation of the intestinal flora or the possibility of therapeutic use of bile acid receptors, and also bariatric surgery. Orv Hetil. 2017; 158(52): 2051-2061.
Recently more and more evidences have emerged about the oncogenic effect of type 2 diabetes and metabolic syndrome. Among these evidences epidemiological data are in first line. There is a causal relationship according to gender, ethnicity and geographic situation between different tumors and type 2 diabetes/metabolic syndrome as well. Supposed pathomechanisms are obesity, cytokines, secreted excessively in adipose tissue, permanent and postprandial hyperglycemia, hyperinsulinism and insulin resistance, other growth factors, like proinsulin, insulin like growth factor-1, reactive oxygen species, angiogenesis, inflammation, and the multiple effects of inflammatory cytokines. It proved to be evident that both peroxisome-proliferator-activated receptors and the regulatory ubiquitin proteasome system have significant role in insulin sensitivity and in co-ordinating cell proliferation and angiogenesis. These mechanisms in metabolic syndrome are risk factors towards atherosclerosis and cancer diseases as well. This newly emerged knowledge may open new pathways in treating and preventing the above-mentioned pathologic processes.
Regulatory role of the brain in energy expenditure, appetite, glucose metabolism, and central effects of insulin has been prominently studied. Certain neurons in the hypothalamus increase or decrease appetite via orexigenes and anorexigenes, regulating energy balance and food intake. Hypothalamus is the site of afferent and efferent stimuli between special nuclei and beta- and alpha cells, and it regulates induction/inhibition of glucose output from the liver. Incretines, produced in intestine and in certain brain cells (brain-gut hormones), link to special receptors in the hypothalamus. Central role of insulin has been proved both in animals and in humans. Insulin gets across the blood-brain barrier, links to special hypothalamic receptors, regulating peripheral glucose metabolism. Central glucose sensing, via "glucose-excited" and "glucose-inhibited" cells have outstanding role. Former are active in hyperglycaemia, latter in hypoglycaemia, via influencing beta- and alpha cells, independently of traditional metabolic pathways. Evidence of brain insulin resistance needs centrally acting drugs, paradigm changes in therapy and prevention of metabolic syndrome, diabetes, cardiovascular and oncological diseases.
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