Metabolic syndrome and its component conditions of hypertension, obesity, and insulin resistance are on the increase in United States. Metabolic syndrome substantially increases the risk of cardiovascular disease and type 2 diabetes (T2D). To date, no published study has examined the relationship between psychological traumas from physical and/or sexual assault in childhood and metabolic syndrome or its components. This study, using the psychoneuroimmunology (PNI) model, investigated associations between psychological trauma (physical/sexual abuse) in childhood and metabolic syndrome in adulthood using data from the Midlife in the United States II (MIDUS-II) study. This research was undertaken to investigate whether a history of psychological trauma was associated with an elevated risk for metabolic syndrome. Chi-square test and logistic regression were used to investigate the respective associations. Metabolic syndrome was the dependent variable, assault in childhood was the independent variable, and the relevant covariates included in the logistic regression model were age, gender, cigarette and alcohol consumption, and ethnicity. While there was no significant association between assault in childhood and metabolic syndrome (p = 0.146), there were significant associations between metabolic syndrome and age group (p =< 0.026). In the adjusted logistic regression model, the only covariate that showed significant association with metabolic syndrome was Age Group 2 (41-55; p = 0.016). Also significant was the association between sexual assault in childhood and high blood pressure (p = 0.041). The results of this study suggest that clinicians may wish to watch for evidence of abuse, given the potential for future health impacts.

Orientador: Camila Renata Corrêa / Banca: Janete Pessuto Simonetti / Banca: Dijon Henrique Salomé de Campos / Banca: Miriam Domingues Cardoso / Banca: Estela Maria Leite Meirelle Monteiro / Resumo: Introdução: A síndrome metabólica (SM) é uma doença atribuída à mudança do estilo de vida a qual tem atingido habitantes de diferentes locais. Objetivo: Investigar a prevalência de síndrome metabólica e fatores associados a ela nos moradores adultos do Arquipélago de Fernando de Noronha (PE-Brasil). Método: Foram avaliados em 363 indivíduos. Idade, medidas antropométricas, pressão arterial sistêmica, e exames bioquímicos foram avaliados. A SM foi diagnosticada de acordo com os critérios da International Diabetes Federation (IDF). Resultados: Dos 363 indivíduos 248 (68,3%) eram do sexo feminino e 115 (31,6 %) do sexo masculino, com a idade média de 43,3 ± 9,1 anos, peso médio de 75,3 ± 16,4kg. A prevalência de SM foi de 20,7%. Dentre os outros fatores associados a ela, a circunferência da cintura mostrou-se bastante elevada na população estudada, 253 indivíduos (69,7%). Quanto a pressão arterial sistêmica, 117 (32,2%) dos indivíduos eram hipertensos, glicemia de jejum alterada foi observada em 68 (18,7%) dos indivíduos, triglicérides em 70 (19,3%), HDLc em 76 (20,9%). A prática de atividade física apresentou-se baixa, apenas 103 (28,4%) praticavam algum tipo de exercício físico e 62 (17%) consumiam frutas e verduras, 47 (12,9%) eram tabagistas, 133 (36,6%) faziam o uso de bebidas alcoólicas e 207 (56,7%) consumiam água dessalinizada. Conclusão: A Síndrome Metabólica diagnosticada na população foi afetada pelo alto índice do aumento da circunferência da cintura, baixo consumo de frutas e verduras e pouca prática de atividade física. A população necessita de um programa abrangente e integrado de educação em saúde, com estímulos para inserir modos preventivos modificando seus hábitos de vida, incentivando o consumo de alimentos saudáveis, visando à conscientização da melhoria de qualidade de vida dos moradores da ilha / Abstract: Introduction: Metabolic syndrome (MS) is a disease attributed to lifestyle change which has affected people from different locations. Objective: To investigate the prevalence of metabolic syndrome and factors associated with it in the adult residents of the archipelago of Fernando de Noronha (PE-Brazil). Method: The study included 363 individuals. Age, anthropometric measures, blood pressure, and biochemical tests were evaluated. MS was diagnosed according to the criteria of the International Diabetes Federation (IDF). Results: Of 363 individuals 248 (68.3%) were female and 115 (31.6%) male, mean age 43.3 ± 9.1 years, mean weight of 75.3 ± 16,4kg. The prevalence of MS was (20.66%). Among the other factors associated with it, waist circumference proved to be very high in the study population, 253 individuals (69.69%). As for blood pressure, 117 (32.23%) individuals were hypertensive, impaired fasting glucose was observed in 68 (18.73%) of subjects, triglycerides by 70 (19.28%), HDL-C 76 (20.93%). The low physical activity presented itself, only 103 (28.37%) practice some form of physical exercise and 62 (17%) consume fruits and vegetables, 47 (12.94%) were smokers, 133 (36.63%) were using alcohol and 207 (56.74%) consumed desalinated water. Conclusion: Metabolic syndrome diagnosed in the population was affected by the high rate of increase in waist circumference, low consumption of fruits and vegetables, little physical activity. The population needs a comprehensive and integrated program of health education, with incentives to enter preventive modes modifying your lifestyle habits by encouraging the consumption of healthy foods, aimed at raising awareness of improved quality of life for residents of the island / Doutor

A reprogramação fenotípica causada por alterações ambientais distintas associada ao alto consumo de frutose na idade adulta poderia contribuir para o agravamento de distúrbios metabólicos. Para avaliar se a exposição pré-natal à dexametasona (DEX) modula os efeitos do consumo de frutose sobre o metabolismo hepático, investigamos a prole masculina nascida de ratas Wistar tratadas ou não com DEX (0,2mg/kg massa corpórea/dia) no 3°período gestacional. As proles de mãe controle (sem tratamento) e mães tratadas com DEX foram mantidas sem frutose (CTL e DEX) ou foram suplementadas com solução de frutose a 10% durante 8 semanas (frutose e DEX+frutose). Tanto os grupos frutose quanto DEX+frutose apresentaram consumo de frutose semelhante, intolerância à glicose e aumento da atividade máxima da enzima glicolítica PFK. Apenas DEX+frutose apresentou aumento dos triglicérides hepáticos e acúmulo de lipídeos intra-hepáticos. Além disso, o grupo DEX+frutose não mostrou expressão aumentada dos genes sec22, mttp e apoB, envolvidos na síntese, montagem e secreção de VLDL; paralelamente, observamos diminuição na concentração de triglicérides em 6 horas após injeção de Tyloxapol comparado ao DEX e frutose. Ainda, apresentou diminuição da expressão de BECLIN1, da expressão gênica de HSP90, e alteração de marcadores moleculares relacionados ao HCC, como diminuição de TP53, P21 e TIGAR, e aumento da expressão de mRNA afp e hsp70. Em conjunto, nossos dados indicam que a exposição à DEX in útero leva a uma resposta metabólica única frente a alta ingestão de frutose na vida adulta. O aumento da gliconeogênese e intolerância à glicose, a redução na produção e secreção de VLDL e o prejuízo no fluxo autofágico estimulam o acúmulo de gotículas lipídicas no fígado que pode favorecer o desenvolvimento de HCC em resposta à alta ingestão de frutose. / Phenotypic programming caused by distinct environmental changes and associated with high fructose consumption in adulthood could contribute to the worsening of metabolic disorders. To evaluate whether prenatal exposure to Dexamethasone (DEX) modulates the effects of fructose consumption on hepatic metabolism, we investigated male offspring born to Wistar rats treated with or without DEX (0.2 mg / kg body weight / day) at 3rd gestational period. The offspring of control (untreated) and DEX treated mothers were maintained without fructose (CTL and DEX) or supplemented with 10% fructose solution for 8 weeks (fructose and DEX+fructose). Both the fructose and DEX+fructose groups showed similar fructose consumption, glucose intolerance and increased maximal activity of the glycolytic enzyme PFK. Only DEX+fructose presented increase in hepatic triglycerides and accumulation of intrahepatic lipids. In addition, the DEX + fructose group did not show increased expression of sec22, mttp and apoB genes involved in the synthesis, assembly and secretion of VLDL; in parallel, we observed a decrease in TG concentration in 6 hours after injection of Tyloxapol, compared to DEX and fructose. In addition, there was a decrease in BECLIN1 expression, HSP90 gene expression, and alteration of HCC-related molecular markers such as TP53, P21 and TIGAR, and increased expression of afp and hsp70 mRNA. Taken together, our data indicate that exposure to DEX in utero leads to a unique metabolic response to high fructose intake in adult life. Increased gluconeogenesis and glucose intolerance, reduction in VLDL production and secretion, and loss of autophagic flow stimulate the accumulation of lipid droplets in the liver, that may favor the development of HCC in response to high fructose intake.

The insulin resistance syndrome [INSR] is associated with increased cardiovascular risk and affects up to 25% of the Australian population. The mechanism underlying the relationship between the INSR and increased cardiovascular risk is controversial. We postulated that perturbations in the renin-angiotensin system [RAS] and endothelium-derived NO may be implicated in the development of early vascular changes in the INSR. Repeated measurements of arterial stiffness [using digital photoplethysmography] and haemodynamic parameters in response to vasoactive medications were used to demonstrate the functional expression of angiotensin II [Ang II] receptors and NO synthase [NOS]. Ang II acts via two main receptor sub-types: the Ang II type 1 [AT1] and Ang II type 2 [AT2] receptors. The AT1 receptor is central to the development of arterial stiffness and endothelial dysfunction. The role of AT2 receptors in humans is controversial but is postulated to counter-act AT1 receptor mediated effects in diseased vascular beds. We demonstrated increased AT1 and AT2 receptor-mediated effects in small to medium-sized arteries of subjects with early INSR [Chapter 6]. In addition, functional expression of AT2 receptors in adult insulin resistant humans [Chapter 5], but not in healthy volunteers [Chapter 4] was demonstrated. AT1 receptor blockade in subjects with early INSR resulted in improvements in vascular function, with a consequent functional down-regulation of AT2 receptors [Chapter 7]. Functional NOS expression was demonstrated to be increased in subjects with early INSR compared with healthy controls [Chapter 6]. This was postulated to be a homeostatic response to counteract early vascular changes in subjects with early INSR. AT1 receptor blockade in these subjects reduced functional NOS expression [Chapter 8]. In conclusion, patients with early INSR represent a model of early disease where early intervention may be able to reverse the process incited by the initial exposure to multiple cardiovascular risk factors. Early vascular changes in these individuals are mediated at least in part, by increased AT1 receptor activity and/or expression, and may be detected by changes in arterial stiffness indices and non-invasive vascular reactivity studies. There is a compensatory increase in AT2 receptor and NOS expression/activity to counter-act these vascular changes.

The insulin resistance syndrome [INSR] is associated with increased cardiovascular risk and affects up to 25% of the Australian population. The mechanism underlying the relationship between the INSR and increased cardiovascular risk is controversial. We postulated that perturbations in the renin-angiotensin system [RAS] and endothelium-derived NO may be implicated in the development of early vascular changes in the INSR. Repeated measurements of arterial stiffness [using digital photoplethysmography] and haemodynamic parameters in response to vasoactive medications were used to demonstrate the functional expression of angiotensin II [Ang II] receptors and NO synthase [NOS]. Ang II acts via two main receptor sub-types: the Ang II type 1 [AT1] and Ang II type 2 [AT2] receptors. The AT1 receptor is central to the development of arterial stiffness and endothelial dysfunction. The role of AT2 receptors in humans is controversial but is postulated to counter-act AT1 receptor mediated effects in diseased vascular beds. We demonstrated increased AT1 and AT2 receptor-mediated effects in small to medium-sized arteries of subjects with early INSR [Chapter 6]. In addition, functional expression of AT2 receptors in adult insulin resistant humans [Chapter 5], but not in healthy volunteers [Chapter 4] was demonstrated. AT1 receptor blockade in subjects with early INSR resulted in improvements in vascular function, with a consequent functional down-regulation of AT2 receptors [Chapter 7]. Functional NOS expression was demonstrated to be increased in subjects with early INSR compared with healthy controls [Chapter 6]. This was postulated to be a homeostatic response to counteract early vascular changes in subjects with early INSR. AT1 receptor blockade in these subjects reduced functional NOS expression [Chapter 8]. In conclusion, patients with early INSR represent a model of early disease where early intervention may be able to reverse the process incited by the initial exposure to multiple cardiovascular risk factors. Early vascular changes in these individuals are mediated at least in part, by increased AT1 receptor activity and/or expression, and may be detected by changes in arterial stiffness indices and non-invasive vascular reactivity studies. There is a compensatory increase in AT2 receptor and NOS expression/activity to counter-act these vascular changes.

The insulin resistance syndrome [INSR] is associated with increased cardiovascular risk and affects up to 25% of the Australian population. The mechanism underlying the relationship between the INSR and increased cardiovascular risk is controversial. We postulated that perturbations in the renin-angiotensin system [RAS] and endothelium-derived NO may be implicated in the development of early vascular changes in the INSR. Repeated measurements of arterial stiffness [using digital photoplethysmography] and haemodynamic parameters in response to vasoactive medications were used to demonstrate the functional expression of angiotensin II [Ang II] receptors and NO synthase [NOS]. Ang II acts via two main receptor sub-types: the Ang II type 1 [AT1] and Ang II type 2 [AT2] receptors. The AT1 receptor is central to the development of arterial stiffness and endothelial dysfunction. The role of AT2 receptors in humans is controversial but is postulated to counter-act AT1 receptor mediated effects in diseased vascular beds. We demonstrated increased AT1 and AT2 receptor-mediated effects in small to medium-sized arteries of subjects with early INSR [Chapter 6]. In addition, functional expression of AT2 receptors in adult insulin resistant humans [Chapter 5], but not in healthy volunteers [Chapter 4] was demonstrated. AT1 receptor blockade in subjects with early INSR resulted in improvements in vascular function, with a consequent functional down-regulation of AT2 receptors [Chapter 7]. Functional NOS expression was demonstrated to be increased in subjects with early INSR compared with healthy controls [Chapter 6]. This was postulated to be a homeostatic response to counteract early vascular changes in subjects with early INSR. AT1 receptor blockade in these subjects reduced functional NOS expression [Chapter 8]. In conclusion, patients with early INSR represent a model of early disease where early intervention may be able to reverse the process incited by the initial exposure to multiple cardiovascular risk factors. Early vascular changes in these individuals are mediated at least in part, by increased AT1 receptor activity and/or expression, and may be detected by changes in arterial stiffness indices and non-invasive vascular reactivity studies. There is a compensatory increase in AT2 receptor and NOS expression/activity to counter-act these vascular changes.

<p>A quart of the of the adult population worldwide have</p><p>metabolic syndrome. A sedentary lifestyle, low physical</p><p>activity, combined with wrong eating habits, stress,</p><p>smoking and psychosocial factors, are the main causes of</p><p>development of the metabolic syndrome. The purpose of</p><p>the literature review was to illuminate the physical</p><p>activity in persons who have the metabolic syndrome, and</p><p>what sort of advice a nurse use in the promotion of</p><p>physical activity. The study was conducted as a literature</p><p>review, including 15 scientific quantitative articles. In ten</p><p>articles, the focus was on physical activity at the</p><p>metabolic syndrome, and five articles focused on various</p><p>forms of counselling for physical activity. The results</p><p>showed that there is a strong correlation between level of</p><p>physical activity and risk of developing metabolic</p><p>syndrome. Increased physical activity reduces the risk of</p><p>developing metabolic syndrome and has positive effects</p><p>on metabolic risk factors. Physical activity may be crucial</p><p>for the prevention of metabolic syndrome. Advice via</p><p>telephone, e-mail and physical activity on prescription is</p><p>effective method for the promotion of physical activity.</p><p>This study also showed that the nurse has an important</p><p>role in promoting physical activity. Promotion of physical</p><p>activity should be given a clearer place in health care.</p>

Thesis (M.Sc. (Nutrition))--North-West University, Potchefstroom Campus, 2007.

BACKGROUND: Risk factors associated with Metabolic Syndrome (MetS) have been implicated in cardiovascular disease (CVD) development and outcomes. Few studies have investigated relationships between psychological variables, MetS factors, and indices of cardiac structure and function (CSF) among healthy individuals in a single conceptual model. No studies to date have analyzed such relationships in patients with CVD. METHODS: The present study examined associations between cynical hostility (CynHo), MetS factors, and CSF in 186 multi-ethnic post-myocardial infarction (MI) patients. Structural equation modeling was used to test a theory driven model of MetS that had good statistical fit. Primary MetS variables included waist circumference (WC), the homeostatic model of insulin resistance (HOMA-IR), glucose area under the curve (G-AUC), triglycerides (TRIG), high-density lipoprotein cholesterol (HDL-C), and diastolic blood pressures (DBP). Secondary MetS variables included plasminogen activator inhibitor-1 (PAI-1) and a latent inflammation variable comprised of CRP and IL-6. Cardiac function variables were fractional shortening (FS), E/A ratio, and rate-pressure product (RPP). A latent cardiac mass (CM) variable was also created. RESULTS: The final structural model had good model fit (Chi-Square(102)=100.65, p=0.52, CFI=1.00, RMSEA=0.00, and SRMR=0.04). Direct paths were supported between WC and CM and all MetS factors except TRIG and G-AUC. WC was indirectly associated with DBP via CM. The model supported positive direct paths between HOMA-IR and G-AUC, TRIG, and PAI-1, but not inflammation or HDL-C. HOMA-IR demonstrated a direct positive association with RPP and direct inverse associations with FS and E/A ratio. No direct paths were supported between other MetS variables except one between TRIG and HDL-C. CynHo demonstrated a direct positive relationship with HOMA-IR. CONCLUSIONS: Similar to findings in healthy individuals, central adiposity and IR play primary roles in CSF impairment in post-MI patients. Findings suggest that CynHo could promote the progression of metabolic dysfunction and cardiac disease via factors that influence the efficiency of glucose metabolism. Interventions for post-MI patients should take into account both direct and indirect effects of CynHo, central adiposity, and IR on the progression of CVD in this population to reduce adverse outcomes and improve quality of life.

Das Metabolische Syndrom stellt eine Kombination verschiedener metabolischer Anomalien in einem Individuum dar. Starkes Übergewicht gilt als maßgebende Größe in der Genese des Syndroms, welches mit einem enormen Risiko für kardiovaskuläre Erkrankungen einhergeht. Um die stark steigende Prävalenz des Metabolischen Syndroms einzudämmen, sind dringend Konzepte für die Behandlung, vor allem jedoch für die Prävention von Übergewicht erforderlich. Einen wichtigen Beitrag leisten diesbezüglich Ballaststoffe in der Ernährung. Sie tragen auf unterschiedlichen Wegen zur Gewichtskontrolle bei und beeinflussen zudem verschiedene mit dem Metabolischen Syndrom assoziierte Blutparameter. Ebenso werden protektive Effekte von Polyphenolen, welche zur Gruppe der sekundären Pflanzenstoffe zählen, beschrieben. Diese wirken u. a. auf den Glukose- sowie den Insulinhaushalt und greifen darüber hinaus in die Regulation der Fettverbrennung sowie des Energieverbrauches ein. Die Kombination beider Substanzgruppen verspricht bedeutendes gesundheitsförderndes Potential; dieses wurde gegenwärtig jedoch kaum untersucht. Carobballaststoff ist ein polyphenolreicher und vorwiegend unlöslicher Extrakt der Frucht des Johannisbrotbaumes (Ceratonia siliqua L). Bislang publizierte Studien zur physiologischen Wirksamkeit dieses Ballaststoffpräparates weisen sowohl beim Tier als auch beim Menschen bemerkenswerte hypocholesterinämische Eigenschaften nach. Inwiefern sich der Verzehr des Carobballaststoffes ebenso auf die Entwicklung von Übergewicht sowie anderen Messgrößen des Metabolischen Syndroms auswirkt, ist allerdings nicht bekannt. Die Zielstellung der Promotionsarbeit bestand darin, die postprandialen Wirkungen des Carobballaststoffverzehrs mit Hilfe einer Humanstudie aufzuzeigen. In die randomisierten, einfach verblindeten Untersuchungen im cross-over-Design wurden 20 gesunde Erwachsene im Alter zwischen 22 und 62 Jahren eingeschlossen. Unter Verwendung variierender Begleitmahlzeiten wurden die postprandialen Effekte verschiedener Mengen des Carobballaststoffes untersucht. Hierbei standen die Veränderungen der Plasmakonzentrationen von Glukose, Triglyceriden (TG), totalem und acyliertem Ghrelin sowie der Serumkonzentrationen von Insulin und nicht-veresterten Fettsäuren (NEFA) im Mittelpunkt der Betrachtungen. Der Verzehr des Carobballaststoffes in Kombination mit 200 ml Wasser und 50 g Glukose erhöhte die postprandialen Glukose- und Insulinkonzentrationen gegenüber der Glukoselösung ohne Ballaststoffzusatz. In Kombination mit 400 ml einer Flüssigmahlzeit verzehrt, senkte Carobballaststoff die postprandialen TG-, NEFA- und Ghrelin- (acyliert) Antworten. Die Untersuchung des respiratorischen Quotienten nach Zusatz von Carobballaststoff zur Flüssigmahlzeit mittels indirekter Respirationskalorimetrie bekräftigte die bereits bekannten Effekte auf den Lipidmetabolismus und wies zudem eine Steigerung der Fettverwertung unter Verminderung der Glukoseoxidation nach. Wurde Carobballaststoff schließlich in Lebensmittel eingebracht, sanken nach dem Verzehr dieser Lebensmittel erneut die postprandialen Konzentrationen an TG und NEFA. Gleichzeitig erhöhten sich die Glukose-, Insulin- sowie Ghrelin- (acyliert) Antworten. Carobballaststoff löst in Abhängigkeit von der jeweils verzehrten Begleitmatrix unterschiedliche Effekte aus. Das Präparat weist beachtliche Wirkungen auf die Blutlipide sowie den Energieverbrauch auf, hat indes ungünstige Wirkungen auf die Blutglukose, sofern er in Kombination mit einer veränderten Nährstoffmatrix aufgenommen wird. Carobballaststoff besitzt starkes gesundheitsförderndes Potential; jedoch sind weitere Studien notwendig, um seine Wirkungen sowie deren Voraussetzungen besser zu verstehen. Ferner sollten Untersuchungen über einen längeren Zeitraum vorgenommen werden, um die langfristige Relevanz der gewonnenen Ergebnisse darzulegen. Danach stellt die Anreicherung spezieller Lebensmittel mit Carobballaststoff einen geeigneten Weg dar, um von den viel versprechenden protektiven Wirkungen des Präparates zu profitieren. / The metabolic syndrome is a clustering of metabolic abnormalities and cardiovascular risk factors that occur in one individual. Since many individuals suffering of the metabolic syndrome are overweight, dietary treatment should primarily focus on weight reduction and control to handle and, much more importantly, to prevent the genesis of the syndrome. Dietary fiber could play a role in the management of the metabolic syndrome through its ability to control body weight as well as several parameters associated to the syndrome. Beside this, dietary polyphenols have been shown to influence glucose and insulin metabolism. Furthermore, studies in mice and men showed that polyphenols might increase fat oxidation and energy expenditure. The combination of both, dietary fiber and polyphenols, may exert beneficial health effects, which are not known up to now. A polyphenol-rich insoluble dietary fiber preparation from carob pulp (Ceratonia siliqua L; carob fiber) showed significant hypocholesterolemic activity in different animal trails and two human studies indicating that carob fiber may have potent health effects. However, short term effects on parameters associated with the control of the metabolic syndrome are not known. Therefore, a study was conducted to investigate the postprandial effects of carob fiber in healthy humans using different background food matrices. The study was designed as a randomized single-blind cross-over study in 20 subjects, aged 22 to 62 years. During several examinations plasma glucose, triglycerides (TG), total and acylated ghrelin, cholecystokinin (CCK) and peptide YY (PYY) as well as serum insulin and non-esterified fatty acids (NEFA) were repeatedly assessed before and after ingestion of carob fiber in combination with different test meals. The study results showed that carob fiber, consumed within a glucose load, increased plasma glucose and serum insulin compared to control. Plasma PYY increased after consumption of carob-enriched glucose solution. In a second part of the study, postprandial changes were assessed before and after ingestion of an isocaloric standardized liquid meal with or without carob fiber. Carob fiber intake lowered acylated ghrelin, triglycerides, and NEFA compared to control meal. Postprandial energy expenditure was increased and RQ was reduced after liquid meal with carob fiber compared to control meal. Finally, effects of the consumption of carob fiber-enriched foods were investigated at the subsequent day. Enrichment of foods increased plasma glucose and acylated ghrelin responses. Plasma triglycerides and serum NEFA responses were lower after bread ingestion compared to control. These results indicate that the effects of polyphenol-rich carob fiber on different blood parameters depend on the meal composition. Carob fiber showed beneficial effects on blood lipids as well as energy homeostasis, but also a deteriorated glycemic control when administered within a different food matrix. Further studies are needed to clarify observed effects and the mechanisms behind. Additionally, present study shows only short-term effects of carob fiber consumption, which might be less pronounced after long-term consumption due to adaptation mechanisms. Thus, future studies should elucidate the relevance of observed effects in long-term.