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Humans carry up to 200 bacterial species in the gastrointestinal tract. Important contribution of these genes is in carbohydrate degradation. The main task of the gut microbiota is digestion of food. The dominant gut bacteria are degradates of complex polysaccharides and releasing SCFA which are the sources for energy, cholesterol synthesis and gluconeogenesis. The mutual interaction of gut microbiota and host immune system is necessary for maintaining their symbiotic relationship. Microbial compositions differ in different metabolic conditions. Firmicutes are dominant in obese subjects while Akkermansia muciniphila which protect against adiposity, low grade inflammation in adipose tissue and insulin resistance is reduced in this population. Intestinal dysbiosis is associated with insulin resistance and diabetes type 2. Betaproteobacteria was highly enriched in diabetic population. The ratio of Bacteriodetes to Firmicutes and the Bacteroides-Prevotella group to the C.coccoides-E.rectale group are reduced. Gastrointestinal rearrangements after RYGB promote substantial changes on the gut microbiota. Gut microbota manipulation in favor of Akkermansia spp. may contribute in antidiabetic effect of metformin and could be potential treatment for T2D. Changes in gut bacteria after RYGB (Roux-en-Y gastric bypass) alter the body weight independent of other effects of bariatric/metabolic surgery. Mechanism for diabetes remission after bariatric surgery is still not clear. Besides change in incretin secretion and bile acid recirculation, potential mechanism is change of gut microbiota content. Possible improvement of glucose regulation following bariatric surgery may be related to butyrate and propionate production by some bacteria species, which influence glucose metabolism independently of bile acids recirculation.

Bariatric surgery is the most efficient treatment for obesity and comorbidities. This treatment modality is the most potent for weight reduction with long-term weight maintenance and positive metabolic effects. The effect on weight loss and possible side effect depends of type of surgery. Micro and macronutrient deficiencies can occur after malapsorptive procedures. Iron deficiency occurs in almost half of patients following RYGB (Roux-en-Y gastric bypass). The main causes of iron deficiency are insufficient meat ingestion and lack of hydrochloric acid after removal of pylorus. B12 deficiency occured 6 months after RYGB in patients with oral supplementation of B12. Bone turnover increased three months after RYGB, and the levels of bone turnover markers increased 200% in next 12-18 months. Impaired vitamin D absorption leads to decreased calcium absorption and secondary hyperparathyroidism with lower bone mineral density. After the bariatric surgery, testosterone level becomes higher and all sexual quality indicators improving. Malapsorptive procedures with nutritive deficiency can cause oligo-astenozooteratospermia and male infertility. Due to the same reason pregnancy is not recommended in the first year bariatric surgery. Possible side effect of pregnancy within 12 months after surgery is fetal growth retardation. There is twice higher incidence for developing alcohol or other addition after bariatric surgery then in non-operated obese patients. The frequency of depressive episodes and suicide attempt is higher after bariatric surgery.

Introduction: pseudohypoparathyroidism (PHP) is hormone resistance syndrome described for the first time in 1942 by Albright et al. All this patients had high levels of the PTH and specific skeletal deformities which were later termed as Albright hereditary osteodystrophy (AHO). The PTH requires the alpha subunit of G protein for its action. GNAS1 gene encodes the alpha subunit of the G protein and molecular defects in this gene lead to the occurrence of at least four different forms of this syndrome. Pseudopseudohypoparathyroidism (PPHP) is a form of PHP which is characterized by physical features of AHO without any evidence of PTH resistance. Albright hereditary osteodystrophy like syndrome (AHO like syndrome) has some common characteristics with AHO but is not connected with the molecular defect in the GNAS 1 gene. Case outline: we reported the case of the female patient with the phenotypic characteristics of AHO (brachydactyly, short stature, mild degree of intelectual deficit and genu varum) but without any evidence of PTH resistance. PPHP occurs mainly in families with PHP 1a and it is inherited from the father which is not the case with our patient. There is a theoretical possibility that the mutation of the GNAS 1 gene occurred de novo but without genetic testing the 2q37 deletion and AHO like syndrome can not be excluded. Conclusion: in same cases of PPHP the diagnosis of AHO like syndrome should be considered but the only way to make the precise diagnosis is the genetic testing as it was in our case.