RESUMO
BACKGROUND: Whether a patient's outcomes are better when receiving nutritional counselling during cardiac rehabilitation (CR) has been scarcely described. We compared changes in weight, waist circumference (WC) and blood pressure (BP) in patients attending CR with and without nutritional counselling. METHODS: A retrospective analytical study was conducted in which two groups of patients who completed a phase II CR (36 sessions) were compared: CONTROL [n = 144, mean (SD) age = 59 (12) years, 17% females], comprising patients without nutritional counselling (attended between 2003 and 2009), and NUT [n = 128, mean (SD) age = 60 (13) years, 27% females], comprising patients with dietitian-delivered nutritional counselling (attended between 2010 and 2019). Repeated-measures analysis of variance was used to compare changes in weight, WC, and BP during CR between groups. Logistic regression models determined the probability of reducing weight and systolic BP (SBP). RESULTS: NUT group decreased weight [-1.3 (3.1) kg; P < 0.0001] and WC [-3.0 (3.8) cm; P < 0.0001] to a greater extent than CONTROL [weight: -0.4 (3.1) kg; P = 0.51; WC: -1.4 (4.5) cm; P = 0.02]. In CONTROL, 7% reduced ≥ 5% weight and 31% reduced ≥ 10 mmHg SBP, whereas, in the NUT group, 18% reduced ≥ 5% weight and 47% reduced ≥ 10 mmHg SBP. Patients in NUT (versus CONTROL) were more likely to lose ≥ 5% of weight (odds ratio = 4.27, 95% confidence interval = 1.69-10.80; P < 0.01) and reduce SBP ≥ 10 mmHg (odds ratio = 3.15, 95% confidence interval = 1.58-6.27; P < 0.01). CONCLUSIONS: Patients who received nutritional counselling during CR improved anthropometric measures and were more likely to lose weight and reduce SBP than patients without nutritional counselling.
Assuntos
Reabilitação Cardíaca , Pressão Sanguínea , Aconselhamento , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Circunferência da CinturaRESUMO
High circulating nonesterified fatty acids (NEFAs) concentration, often reported in diabetes, leads to impaired glucose-stimulated insulin secretion (GSIS) through not yet well-defined mechanisms. Serotonin and dopamine might contribute to NEFA-dependent ß-cell dysfunction, since extracellular signal of these monoamines decreases GSIS. Moreover, palmitate-treated ß-cells may enhance the expression of the serotonin receptor Htr2c, affecting insulin secretion. Additionally, the expression of monoamine-oxidase type B (Maob) seems to be lower in islets from humans and mice with diabetes compared to nondiabetic islets, which may lead to increased monoamine concentrations. We assessed the expression of serotonin- and dopamine-related genes in islets from db/db and wild-type (WT) mice. In addition, the effect of palmitate and oleate on the expression of such genes, 5HT content, and GSIS in MIN6 ß-cell was determined. Lower Maob expression was found in islets from db/db versus WT mice and in MIN6 ß-cells in response to palmitate and oleate treatment compared to vehicle. Reduced 5HT content and impaired GSIS in response to palmitate (-25%; p < 0.0001) and oleate (-43%; p < 0.0001) were detected in MIN6 ß-cells. In conclusion, known defects of GSIS in islets from db/db mice and MIN6 ß-cells treated with NEFAs are accompanied by reduced Maob expression and reduced 5HT content.
Assuntos
Células Secretoras de Insulina/efeitos dos fármacos , Ilhotas Pancreáticas/metabolismo , Transcriptoma/genética , Acetilserotonina O-Metiltransferasa/efeitos dos fármacos , Acetilserotonina O-Metiltransferasa/genética , Animais , Arilalquilamina N-Acetiltransferase/efeitos dos fármacos , Arilalquilamina N-Acetiltransferase/genética , Catecol O-Metiltransferase/efeitos dos fármacos , Catecol O-Metiltransferase/genética , Linhagem Celular , Dopa Descarboxilase/efeitos dos fármacos , Dopa Descarboxilase/genética , Proteínas da Membrana Plasmática de Transporte de Dopamina/efeitos dos fármacos , Proteínas da Membrana Plasmática de Transporte de Dopamina/genética , Dopamina beta-Hidroxilase/efeitos dos fármacos , Dopamina beta-Hidroxilase/genética , Insulina/metabolismo , Secreção de Insulina , Células Secretoras de Insulina/metabolismo , Camundongos , Monoaminoxidase/efeitos dos fármacos , Monoaminoxidase/genética , Ácido Oleico/farmacologia , Ácido Palmítico/farmacologia , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Serotonina/metabolismo , Proteínas da Membrana Plasmática de Transporte de Serotonina/efeitos dos fármacos , Proteínas da Membrana Plasmática de Transporte de Serotonina/genética , Transcriptoma/efeitos dos fármacos , Triptofano Hidroxilase/efeitos dos fármacos , Triptofano Hidroxilase/genética , Tirosina 3-Mono-Oxigenase/efeitos dos fármacos , Tirosina 3-Mono-Oxigenase/genéticaRESUMO
Pancreatic beta cells sense glucose flux and release as much insulin as required in order to maintain glycaemia within a narrow range. Insulin secretion is regulated by many factors including glucose, incretins, and sympathetic and parasympathetic tones among other physiological factors. To identify the mechanisms linking obesity-related insulin resistance with impaired insulin secretion represents a central challenge. Recently, it has been argued that a crosstalk between skeletal muscle and the pancreas may regulate insulin secretion. Considering that skeletal muscle is the largest organ in non-obese subjects and a major site of insulin- and exercise-stimulated glucose disposal, it appears plausible that muscle might interact with the pancreas and modulate insulin secretion for appropriate peripheral intracellular glucose utilization. There is growing evidence that muscle can secrete so-called myokines that can have auto/para/endocrine actions. Although it is unclear in which direction they act, interleukin-6 seems to be a possible muscle-derived candidate protein mediating such inter-organ communication. We herein review some of the putative skeletal muscle-derived factors mediating this interaction. In addition, the evidence coming from in vitro, animal and human studies that support such inter-organ crosstalk is thoroughly discussed.
Assuntos
Glucose/metabolismo , Resistência à Insulina , Células Secretoras de Insulina/metabolismo , Insulina/metabolismo , Músculo Esquelético/metabolismo , Obesidade/metabolismo , Pâncreas/metabolismo , Humanos , Incretinas/metabolismo , Secreção de Insulina , Receptor Cross-TalkRESUMO
Active skeletal muscle synthesizes and releases interleukin-6 (IL-6), which plays important roles in the organism's adaptation to exercise. Autocrine/paracrine ATP signaling has been shown to modulate IL-6 expression. The aim of this study was to determine whether a period of physical activity modifies the ATP-induced IL-6 expression. BalbC mice were either subject to 5 weeks voluntary wheel running (VA) or kept sedentary (SED). Flexor digitorum brevis muscles were dissected, stimulated with different ATP concentrations (0-100 µM) and IL-6 mRNA levels were measured using qPCR. ATP evoked a concentration-dependent rise in IL-6 mRNA in both SED and VA mice. VA mice however, had significantly higher ATP sensitivity (pD2 pharmacological values: VA=5.58±0.02 vs. SED=4.95±0.04, p<0.05). Interestingly, in VA mice we observed a positive correlation between the level of physical activity and the IL-6 mRNA increase following fiber stimulation with 10 µM ATP. In addition, there were lower P2Y2- and higher P2Y14-receptor mRNA levels in skeletal muscles of VA compared to SED mice, showing plasticity of nucleotide receptors with exercise. These results suggest that exercise increases skeletal muscle ATP sensitivity, a response dependent on the level of physical activity performed. This could have an important role in the mechanisms controlling skeletal muscle adaptation to exercise and training.
Assuntos
Trifosfato de Adenosina/metabolismo , Interleucina-6/metabolismo , Fibras Musculares Esqueléticas/metabolismo , Corrida/fisiologia , Adaptação Fisiológica , Tecido Adiposo/metabolismo , Animais , Comunicação Autócrina/fisiologia , Índice de Massa Corporal , Citrato (si)-Sintase/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Miocárdio/metabolismo , Condicionamento Físico Animal , RNA Mensageiro/metabolismo , Receptores Purinérgicos P2Y/metabolismoRESUMO
AIMS/HYPOTHESIS: Insulin resistance is characterised by impaired glucose utilisation when measured by a euglycaemic-hyperinsulinaemic clamp. We hypothesised that, in response to postprandial conditions, non-diabetic individuals would have similar intracellular glycolytic and oxidative glucose metabolism independent of the degree of insulin resistance. METHODS: Fourteen (seven male) sedentary, insulin-sensitive participants (mean ± SD: BMI 25 ± 4 kg/m²; age 39 ± 10 years; glucose disposal rate 9.4 ± 2.1 mg [kg estimated metabolic body size]⻹ min⻹) and 14 (six male) sedentary, non-diabetic, insulin-resistant volunteers (29 ± 4 kg/m²; 34 ± 13 years; 5.3 ± 1.2 mg [kg estimated metabolic body size]⻹ min⻹) received after a 10 h fast 60 g glucose plus 15 g [6,6-²H2]glucose. Serum glucose and insulin concentrations, plasma ²H enrichment and whole-body gas exchange were determined before glucose ingestion and hourly thereafter for 4 h. Plasma ²H2O production is an index of glycolytic disposal. On day 2, participants received a weight-maintenance diet. On day 3, a euglycaemic-hyperinsulinaemic clamp was performed. RESULTS: Insulin-resistant individuals had about a twofold higher postprandial insulin response than insulin-sensitive individuals (p = 0.003). Resting metabolic rate was similar in the two groups before (p = 0.29) and after (p = 0.33-0.99 over time) glucose ingestion, whereas a trend for blunted glucose-induced thermogenesis was observed in insulin-resistant vs insulin-sensitive individuals (p = 0.06). However, over the 4 h after the 75 g glucose ingestion, glycolytic glucose disposal was the same in insulin-sensitive and insulin-resistant individuals (36.5 ± 3.7 and 36.2 ± 6.4 mmol, respectively; p = 0.99). Similarly, whole-body carbohydrate oxidation did not differ between the groups either before or after glucose ingestion (p = 0.41). CONCLUSIONS/INTERPRETATION: Postprandial hyperinsulinaemia and modest hyperglycaemia overcome insulin resistance by enhancing tissue glucose uptake and intracellular glucose utilisation.
Assuntos
Glucose/metabolismo , Glicólise , Resistência à Insulina , Adulto , Metabolismo Basal , Glicemia/análise , Deutério , Feminino , Técnica Clamp de Glucose , Humanos , Hiperglicemia/sangue , Hiperglicemia/metabolismo , Hiperglicemia/fisiopatologia , Hiperinsulinismo/sangue , Hiperinsulinismo/metabolismo , Hiperinsulinismo/fisiopatologia , Insulina/sangue , Masculino , Pessoa de Meia-Idade , Fosforilação Oxidativa , Período Pós-Prandial , Índice de Gravidade de Doença , Termogênese , Adulto JovemRESUMO
The purpose of this review was to examine the role of glycaemic index in fuel partitioning and body composition with emphasis on fat oxidation/storage in humans. This relationship is based on the hypothesis postulating that a higher serum glucose and insulin response induced by high-glycaemic carbohydrates promotes lower fat oxidation and higher fat storage in comparison with low-glycaemic carbohydrates. Thus, high-glycaemic index meals could contribute to the maintenance of excess weight in obese individuals and/or predispose obesity-prone subjects to weight gain. Several studies comparing the effects of meals with contrasting glycaemic carbohydrates for hours, days or weeks have failed to demonstrate any differential effect on fuel partitioning when either substrate oxidation or body composition measurements were performed. Apparently, the glycaemic index-induced serum insulin differences are not sufficient in magnitude and/or duration to modify fuel oxidation.
Assuntos
Composição Corporal/fisiologia , Metabolismo Energético/fisiologia , Índice Glicêmico , Área Sob a Curva , Glicemia/metabolismo , Peso Corporal/fisiologia , Humanos , Insulina/metabolismo , Secreção de Insulina , Consumo de OxigênioRESUMO
BACKGROUND: Glycemic index is hypothesized to determine fuel partitioning through serum plasma insulin modifications induced by dietary carbohydrates, thereby modulating fat accretion or oxidation. OBJECTIVE: To assess the glycemic effects on postprandial fuel oxidation and blood response. DESIGN: In all, 12 obese women were fed on a randomized crossover design with two test meals (breakfast+lunch). High- or low-glycemic meals were provided on separate days. Energy intake on high-glycemic meal was 7758+/-148 kJ and for low-glycemic meal was 7806+/-179 kJ. Carbohydrates supplied were 273+/-5 and 275+/-6 g, respectively. Macronutrient distribution was 55% carbohydrates, 30% fat and 15% protein. Fuel oxidation was measured continuously in a respiratory chamber for 10 h. Serum glucose, free fatty acids (FFA), insulin and glucagon samples were taken for 5 h after breakfast. RESULTS: Glucose AUC changed significantly in response to different glycemic breakfast. Low- vs high-glycemic breakfast was 211+/-84 and 379+/-164 mmol/l (P<0.05). Similarly, insulin changed from 94+/-37 and 170+/-87 nmol/l (P<0.05), respectively. The rate of increment for serum glucose and insulin reached by the high- vs low-glycemic meal was 1.8 times more with the high-glycemic breakfast. Serum FFA were similarly suppressed by both meal types by 3 h after meal intake, but then raised significantly more with the low-glycemic meal by the fourth and fifth hour (P<0.05). Plasma glucagon did not show a significant variation with glycemic index. Carbohydrate and fat oxidation was not modified by glycemic meal characteristics, being virtually the same for low- vs high-glycemic comparisons in the 5 h following breakfast and lunch (P=NS). CONCLUSION: This study demonstrates that dietary glycemic characteristics were unable to modify fuel partitioning in sedentary obese women.