BACKGROUND: Bariatric surgery is the most effective treatment for morbid obesity and type 2 diabetes. Hypercortisolism in patients undergoing bariatric surgery may reduce the effectiveness of surgery and increase the risk of complications. AIM: To assess the prevalence and clinical forms of hypercortisolism in patients with morbid obesity and type 2 diabetes mellitus undergoing examination before bariatric interventions.MATERIALS AND METHODS: Screening for Cushing's syndrome was performed in patients with morbid obesity and type 2 diabetes mellitus referred to the clinic for examination before bariatric surgery. The overnight dexamethasone suppressive test with 1 mg dexamethasone (1-mg DST) was used as a first-line test. Additional tests included 24-hour urinary free cortisol excretion and evening cortisol level in saliva or blood serum. In case of pathological results of the second-line tests, the ACTH level was measured, and suppressive test with 8 mg dexamethasone was performed.RESULTS: The study included 91 patients, 21 men and 70 women, aged 27 to 66 years. A decrease in the cortisol level <50 nmol/l in the 1-mg DST was recorded in 75 patients. In the remaining subjects, the cortisol concentration exceeded the cutoff point, which required further tests. In 14 patients (15.4%) with functional hypercortisolism (pseudo-Cushing`s syndrome), the cortisol level in 1-mg DST ranged from 50 to 140 nmol/l (median 67.7). In three women, the cortisol level in the 1-mg DST demonstrated very high values (593, 461 and 425 nmol/l). During further examination, pituitary adenomas were verified in two of them, and the third woman was diagnosed with adenomas in both adrenal glands.CONCLUSION: The obtained results confirm the need for screening for hypercortisolism in all patients with morbid obesity and type 2 diabetes scheduled for bariatric surgery.
BACKGROUND: Binge eating disorder (BED) is the most prevalent eating disorder manifesting as episodes with higher than usual food intake uncontrolled by patients. Nutritional specifics, their associations with biological and psychological parameters in Type 2 diabetes mellitus (T2DM) with BED have not been studied.AIM: To identify specific characteristics of nutrition (food choices, food planning, diet barriers [DB]) in T2DM patients with and without BED, their associations with clinical, laboratory, and psychological parameters and their changes over time under treatment of BED.MATERIAL AND METHODS: T2DM patients with and without BED participated in this cross-sectional study. In those with and without BED, we compared the characteristics of nutritional style, clinical, laboratory and psychological parameters (depression, anxiety/anxiousness, some personality characteristics, including alexithymia, and diabetes-dependent quality of life (Qol). In subsequent prospective open-label interventional part of the study, we evaluated changes of the nutrition characteristics in T2DM patients with BED under treatment with glucagon-like peptide I receptor agonists (GLP1-RA) versus no BED treatment. The univariate analysis was performed at α=0,05, logistic regression at α=0,10.RESULTS: The study recruited 273 T2DM patients (176 with and 97 without BED). The BED patients ate less frequently than those without: minimal number of daily food intakes 2,6±1,1 and 2,9±0,8, respectively (р=0,010), food intake skipped 1,5±1,8 and 0,8±1,5 weekly (р=0,001). Compared to no-BED patients, those with BED consumed more sweets (р=0,003), “hidden” fats (eggs, р=0,015; nuts, р=0,027), and alcoholic drinks (р=0,004). In the BED group, there were 23 associations between various foods and clinical and laboratory parameters (9 of them indicated favorable and 14 unfavorable food effects). In the non-BED group, 6 associations were found, all them indicating favorable food effects. In both groups, the most significant DB was “difficult to withdraw sweets”. The BED-specific weighted DB were: “difficult to stick to a diet in unexpected situations”, “when I eat more than allowed, I feel bad”, “sometimes I am not allowed to eat being hungry”, and “I would like to eat foods that I should not eat”. Only in the BED group, there were weak but significant correlations between DB numbers/patient and metabolic parameters: НbA1c (r=0,210, р<0,010), serum insulin level (r=0,171, р<0,05), HOMA insulin resistance index (r=0,286, р<0,010), and triglyceride levels (r=0,183, р=0,026). In both groups, DB numbers correlated to higher scores of somatic complaints, alexithymia, depression, psychopathic deviate, paranoia, autism, social introversion, and poorer diabetes-dependent QoL. Logistic regression showed associations of BED to alcoholic intake (odds ratio [OR] 1,03, 95% CI 1,001–1,058, р=0,044), DB domain “limited food diversity” (OR 1,51; 1,172–1,946, р=0,001), food planning (OR 0,154, 0,054–0,442, р=0,001), DB domain “additional food-related costs” (OR 0,49, 0,304–0,792, р=0,004), and high-fiber foods consumption (OR 0,58, 0,324–1,026, р=0,061).In the second 6-month study period with 66/176 BED patients, 33 of them were prescribed GLP1-RAs and 33 continued their previous therapy. In both groups, food choices remained unchanged qualitatively. Under treatment with GLP1-RA, there was statistically significant (but not clinically meaningful) decrease in DB domains “limited foods choices” and “limited foods diversity”, while in the control group, a decrease in “limited foods choices” score and an increase in “additional food-related costs” were found.CONCLUSION: Specific characteristics of nutrition in T2DM patients with BED (less regular food intake, higher intake of unhealthy products and higher numbers of DB, compared to those in T2DM without BED) may negatively affect clinical, laboratory and psychological parameters. Three factors related to nutrition style are associated with increased BED risk and three, with lower risk. The results necessitate a personalized dietary approach to T2DM patients with BED, which requires its timely diagnosis made in primary and secondary care. GLP1-RAs exert no clinically valuable effects on the studied nutrition characteristics in BED patients with T2DM.
BACKGROUND: Adipose tissue (AT) is an active endocrine organ that produces biologically active molecules — adipokines, which participate in lipid and glucose metabolism. The imbalance of adipokine secretion in obesity is a consequence of AT dysfunction, which at the molecular genetic level is manifested as changes in the expression of the key genes, and can be complicated by the development of metabolic disorders, in particular type 2 diabetes mellitus (T2DM).AIM: The aim of this study was to investigate the expression level of PPARG, ADIPOQ, LEP, SLC2A4 genes in subcutaneous and visceral adipose tissue (SAT and VAT) in bariatric patients with obesity and T2DM, as well as to assess the correlation of adiponectin and leptin serum concentrations with the expression of corresponding genes.MATERIALS AND METHODS: The single-center, cross-sectional, two-sample, comparative, observational case-control study included patients with grade II, III, IV obesity with/without T2DM, as well as non-obese individuals who applied to the Pavlov First Saint Petersburg State Medical University for bariatric (patients) and planned abdominal surgeries (control group), SAT and VAT samples, as well as blood serum, were collected. Real-time polymerase chain reaction was used to determine the mRNA levels of target genes in AT. Adiponectin and leptin serum concentrations were assesed by enzyme immunoassay.RESULTS: The group of bariatric patients included 53 patients (mean age 44.1±11.2 years; body mass index (BMI) over 35 kg/m2), including 26 patients with a diagnosis of T2DM and 27 without T2DM. The control group included 15 individuals without obesity, metabolic disorders and T2DM (mean age 46.7±12.8; BMI less than 30 kg/m2). In patients with obesity and T2DM, a decrease in the level of PPARG, ADIPOQ and SLC2A4 gene expression in SAT was observed compared to the control group. The level of PPARG and ADIPOQ gene expression was also reduced in VAT in patients with obesity and T2DM compared to the control group. The observed changes in gene expression in obesity were associated with a decrease in adiponectin and an increase in leptin serum concentrations, with the most pronounced decrease in adiponectin concentration in patients with obesity and T2DM. Unidirectional positive correlations were observed in the expression levels of PPARG, ADIPOQ, LEP, SLC2A4 genes in SAT and VAT in the total cohort.CONCLUSION: The development of T2DM on the basis of obesity and BMI of more than 35 kg/m2 is associated with reduced expression levels of the PPARG, ADIPOQ and SLC2A4 genes in SAT, a marked decrease in the concentration of adiponectin and an increase in the concentration of leptin in the blood serum.
Diabetes mellitus is one of the most pressing problems of modern medicine, characterized by high morbidity (with continuous growth), a decrease in the duration and quality of life, numerous and severe complications. Among the disorders observed in diabetes mellitus, the insufficiency of angiogenesis, the process of formation of new vessels from existing ones, is noted. This process plays an important role in reparative regeneration, ensuring the formation of granulation tissue. The insufficiency of angiogenesis in diabetes mellitus causes a decrease in the rate and quality of wound healing in such patients. We conducted a literature review with the following objectives: to collect up-to-date data on the mechanisms of angiogenesis and its regulation, to identify the links of angiogenesis that are subject to the pathological influence of diabetes mellitus; and to identify potential targets of pharmacological therapy that can compensate for this effect. The results of this work will allow us to apply the data obtained in studies aimed at developing a personalized approach to the management of patients with diabetes mellitus.
Prader–Willi–like syndromes (PWLS) represent a heterogeneous group of disorders characterized by a set of key clinical features, including muscular hypotonia, obesity, psychomotor and speech developmental delay, and behavioral problems, in the absence of methylation abnormalities within the chromosomal region 15q11.2q13. The phenotypic manifestations of PWLS show substantial overlap with the classical Prader–Willi syndrome (PWS), a disorder belonging to the group of imprinting disorders. PWLS include certain chromosomal syndromes (deletions of 1p36, 2pter, 3p26.3, 6q, 10q26, 19p, subtelomeric deletion of 12q, paracentric inversion Xq26q28, Xq27–qter disomy, duplications of 6q, 15q, Xq21.1q21.31, Xq23q25), imprinting disorders (Angelman syndrome, Temple syndrome, pseudohypoparathyroidism types 1A and 1C, pseudopseudohypoparathyroidism, Schaaf–Yang syndrome), and monogenic syndromic forms of obesity (Fragile X syndrome, Bardet–Biedl syndrome, Alström syndrome, Cohen syndrome, Börjeson–Forssman–Lehmann syndrome, MYT1L-related syndrome, SIM1-associated PWS-like obesity, GNAI1-associated neurodevelopmental disorder). The combination of the genetic heterogeneity of PWLS and the absence of the specific genetic defect observed in PWS creates significant challenges for differential diagnosis in clinical practice. This literature review systematizes current research data aimed at refining the phenotypic characterization, management approaches, and treatment strategies for syndromes within the Prader–Willi–like spectrum.
