Phase Angle, Inflammation, and Sarcopenia in Late Postoperative Roux-En-Y Gastric Bypass.

Sarcopenic obesity is characterized by a disproportion between the amount of muscle to fat. Contrary to most studies evaluating parameters related to sarcopenic obesity in the elderly, this study aims to evaluate the phase angle (PhA) and sarcopenia in young individuals pre- and post-Roux-en-Y gastric bypass. A total of 69 volunteers (46 women and 23 men; 38.5 ± 8.1 years) participated in this study. Body composition and PhA were assessed using BIA. Sarcopenia was assessed using a handgrip strength test (HGS) and gait speed (GS), and appendicular lean mass (ALM) was assessed using Dual Energy X-ray Absorptiometry (DXA). The PhA was significantly lower (p < 0.0007) and the resistance (R) significantly higher (p = 0.0026) in the postoperative group. HGS was negatively correlated with R (r = -0.63669; p < 0.0001), hs-CRP (r = -0.45436; p = 0.0197), and leptin (r = -0.46505; p = 0.0043). GS was negatively correlated with R (r = -0.36220; p = 0.0254), and ALM was negatively correlated with reactance (r = -0.49485; p = 0.0034) and R (r = -0.65797; p ≤ 0.0001). PhA and other components of BIA provide a good correlation with sarcopenia, especially regarding the reduction in muscle function, in an early form, in individuals in the pre- and postoperative period of gastric bypass.

Childhood-Onset GH Deficiency versus Adult-Onset GH Deficiency: Relevant Differences Regarding Insulin Sensitivity.

The results of the studies on the pattern of insulin sensitivity (IS) are contradictory in patients with GH deficiency (GHD); however, the interference of the GHD onset stage, childhood or adulthood in the IS has not been assessed by euglycemic hyperinsulinemic clamp (EHC), a gold-standard method for the assessment of insulin sensitivity. In a prospective cross-sectional study, we assessed IS and body composition in 17 adults with hypopituitarism without GH replacement, ten with childhood-onset (COGHD) and seven with adulthood-onset (AOGHD) and compared them to paired control groups. COGHD presented higher IS (p = 0.0395) and a similar percentage of fat mass (PFM) to AOGHD. COGHD showed higher IS than the control group (0.0235), despite a higher PFM (0.0022). No differences were found between AODGH and the control group. In AOGHD and the control group, IS was negatively correlated with PFM (rs: −0.8214, p = 0.0234 and rs: −0.3639, p < 0.0344), while this correlation was not observed with COGHD (rs: −0.1152, p = 0.7514). Despite the higher PFM, patients with COGHD were more sensitive to insulin than paired healthy individuals, while patients with AOGHD showed similar IS compared to controls. The lack of GH early in life could modify the metabolic characteristics of tissues related to the glucose metabolism, inducing beneficial effects on IS that persist into adulthood. Thus, the glycometabolic findings in patients with COGHD seems to be not applicable to AOGHD.

Effects of acute NEFA manipulation on incretin-induced insulin secretion in participants with and without type 2 diabetes.

AIMS/HYPOTHESIS: Incretin effect-the potentiation of glucose-stimulated insulin release induced by the oral vs the i.v. route-is impaired in dysglycaemic states. Despite evidence from human islet studies that NEFA interfere with incretin function, little information is available about the effect in humans. We tested the impact of acute bidirectional NEFA manipulation on the incretin effect in humans. METHODS: Thirteen individuals with type 2 diabetes and ten non-diabetic volunteers had a 3 h OGTT, and, a week later, an i.v. isoglycaemic glucose infusion (ISO; OGTT matched). Both pairs of studies were repeated during an exogenous lipid infusion in the non-diabetic volunteers, and following acipimox administration (to inhibit lipolysis) in people with diabetes. Mathematical modelling of insulin secretion dynamics assessed total insulin secretion (TIS), beta cell glucose sensitivity (ß-GS), glucose-induced potentiation (PGLU) and incretin-induced potentiation (PINCR); the oral glucose sensitivity index was used to estimate insulin sensitivity. RESULTS: Lipid infusion increased TIS (from 61 [interquartile range 26] to 78 [31] nmol/m2 on OGTT and from 29 nmol/m2 [26] to 57 nmol/m2 [30] on ISO) and induced insulin resistance. PINCR decreased from 1.6 [1.1] to 1.3 [0.1] (p < 0.05). ß-GS, PGLU and glucagon, glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP) responses were unaffected. Acipimox (lowering NEFA by ~55%) reduced plasma glucose and TIS and enhanced insulin sensitivity, but did not change ß-GS, PINCR, PGLU or glucagon, GLP-1 or GIP responses. As the per cent difference, incretin effect was decreased in non-diabetic participants and unchanged in those with diabetes. CONCLUSIONS/INTERPRETATION: Raising NEFA selectively impairs incretin effect and insulin sensitivity in non-diabetic individuals, while acute NEFA reduction lowers plasma glucose and enhances insulin sensitivity in people with diabetes but does not correct the impaired incretin-induced potentiation.

Reduced insulin sensitivity in differentiated thyroid cancer patients with suppressed TSH.

OBJECTIVE: TSH-suppression is a therapy for thyroid cancer management, but it may lead to adverse effects, which should be balanced with its benefits. Previous studies evaluating the consequences of TSH suppression on insulin sensitivity have only been done with indirect techniques, and results were controversial. Therefore, we aimed to assess insulin sensitivity in patients with thyroid cancer and suppressed thyroid-stimulating hormone (TSH) with the most appropriate direct method (hyperinsulinemic-euglycemic clamp) in order to get a more conclusive response about the topic. METHODS: A group of 20 non-obese and non-diabetic thyroid cancer patients with suppressed TSH underwent a hyperinsulinemic-euglycemic clamp to evaluate insulin sensitivity. Their results were compared to the results of a sex and body mass index (BMI) -paired control group composed of 20 healthy volunteers. RESULTS: Patients were all female, aged 36.8 ± 10.2 years-old, with mean TSH 0.1 ± 0.1 µIU/mL and mean BMI 26.2 ± 3.3 kg/m2. Insulin sensitivity, determined by the insulin-stimulated glucose uptake (M-value), was lower in the patients group (4.2 ± 1.6 mg/min*kg versus 5.8 ± 1.7, age-adjusted p-value = 0.0205). CONCLUSION: This study shows for the first time that subclinical thyrotoxicosis in patients with thyroid cancer is associated with insulin resistance, as measured by hyperinsulinemic-euglycemic clamp technique. Such finding may be taken into consideration by clinicians when balancing risks and benefits of TSH-suppression therapy in thyroid cancer patients.

Evaluation of patients with head and neck cancer performing standard treatment in relation to body composition, resting metabolic rate, and inflammatory cytokines.

BACKGROUND: Squamous cell carcinoma of the head and neck (SCCHN) usually emerges as a set of signs and symptoms that, either alone or in combination with standard treatment, may lead to malnutrition and weight loss. METHODS: This study evaluated patients with SCCHN before day 0 and 30 days after the end of treatment, with/without tumor resection. Each individual patient underwent analyses of body composition and resting metabolic rate, as well as assessment of serum glucose, insulin, leptin, adiponectin, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), IL-1ß, and insulin sensitivity. RESULTS: There was body mass loss during treatment and significant reduction in body fat and free fat mass. Early nutritional monitoring and tumor resection before treatment led to a better nutritional status and reduced inflammatory state. CONCLUSION: Early nutritional monitoring and resection of the tumor by surgery may be important factors for patients to better tolerate treatment.

Association between prehypertension, metabolic and inflammatory markers, decreased adiponectin and enhanced insulinemia in obese subjects.

BACKGROUND: Obesity is associated with development of the cardiorenal metabolic syndrome, which is a constellation of risk factors, such as insulin resistance, inflammatory response, dyslipidemia, and high blood pressure that predispose affected individuals to well-characterized medical conditions such as diabetes, cardiovascular and kidney chronic disease. The study was designed to establish relationship between metabolic and inflammatory disorder, renal sodium retention and enhanced blood pressure in a group of obese subjects compared with age-matched, lean volunteers. METHODS: The study was performed after 14 h overnight fast after and before OGTT in 13 lean (BMI 22.92 ± 2.03 kg/m(2)) and, 27 obese (BMI 36.15 ± 3.84 kg/m(2)) volunteers. Assessment of HOMA-IR and QUICKI index were calculated and circulating concentrations of TNF-α, IL-6 and C-reactive protein, measured by immunoassay. RESULTS: THE STUDY SHOWS THAT A HYPERINSULINEMIC (HI: 10.85 ± 4.09 µg/ml) subgroup of well-characterized metabolic syndrome bearers-obese subjects show higher glycemic and elevated blood pressure levels when compared to lean and normoinsulinemic (NI: 5.51 ± 1.18 µg/ml, P < 0.027) subjects. Here, the combination of hyperinsulinemia, higher HOMA-IR (HI: 2.19 ± 0.70 (n = 12) vs. LS: 0.83 ± 0.23 (n = 12) and NI: 0.98 ± 0.22 (n = 15), P < 0.0001) associated with lower QUICKI in HI obese when compared with LS and NI volunteers (P < 0.0001), suggests the occurrence of insulin resistance and a defect in insulin-stimulated peripheral action. Otherwise, the adiponectin measured in basal period was significantly enhanced in NI subjects when compared to HI groups (P < 0.04). The report also showed a similar insulin-mediated reduction of post-proximal urinary sodium excretion in lean (LS: 9.41 ± 0.68% vs. 6.38 ± 0.92%, P = 0.086), and normoinsulinemic (NI: 8.41 ± 0.72% vs. 5.66 ± 0.53%, P = 0.0025) and hyperinsulinemic obese subjects (HI: 8.82 ± 0.98% vs. 6.32 ± 0.67%, P = 0.0264), after oral glucose load, despite elevated insulinemic levels in hyperinsulinemic obeses. CONCLUSION: In conclusion, this study highlights the importance of adiponectin levels and dysfunctional inflammatory modulation associated with hyperinsulinemia and peripheral insulin resistance, high blood pressure, and renal dysfunction in a particular subgroup of obeses.

Determining the C-reactive protein level in patients with different clinical forms of chagas disease.

Chagas disease is caused by Trypanosoma cruzi and remains a health problem in the developing countries of South America. The condition leads to cardiac conduction disturbances and chronic heart failure. In this study, 136 individuals were evaluated by the Chagas Disease Study Group of the Hospital de la Universidad Estatal de Campinas in Brazil to determine the relationship between chronic heart failure and the serum C-reactive protein (CRP) level. When patients were stratified according to the different clinical presentations of Chagas disease, it was found that the CRP levels in those with severe heart disease and non-Chagasic cardiopathy were significantly higher than in controls or those with mild heart disease (P< .05), even when participants were stratified by age (i.e. <40 and > or =40 years). There was a direct linear correlation between age and CRP level, such that the older the individual, the higher the CRP level. These data provide further evidence for an association between chronic inflammation and the development of heart failure. Although CRP elevations are not exclusively related to Chagas disease, the CRP level may be a useful marker for the progression of Chagas disease to a more advanced phase.

Metástase óssea de carcinoma cutâneo: relato de um caso / Bone mestastasis of cutaneous carcinoma: a case report

Apresenta-se o caso de um paciente de carcinoma basocelular com acometimento neoplásico tardio da segunda vértebra lombar, cujo diagnóstico foi de carcinoma baso-epidermóide