17 research outputs found

    Hypoglycemia

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    Glucose is an essential metabolic substrate of all mammalian cells being the major carbohydrate presented to the cell for energy production and also many other anabolic requirements. Hypoglycemia is a disorder where the glucose serum concentration is usually low. The organism usually keeps the glucose serum concentration in a range of 70 to 110 mL/dL of blood. In hypoglycemia the glucose concentration normally remains lower than 50 mL/dL of blood. This book provides an abundance of information for all who need them in order to help many people worldwide

    Molecular mechanisms of hyperinsulinemia in obesity

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    Treballs Finals de Grau de Nutrició Humana i Dietètica, Facultat de Farmàcia i Ciències de l'Alimentació, Campus de l'Alimentació de Torribera, Universitat de Barcelona. Curs: 2022-2023. Tutor: Carme Caelles Franch[eng] Obesity-associated insulin resistance and hyperinsulinemia are two interrelated health conditions that have become increasingly prevalent in recent years. For many years, it has been thought that hyperinsulinemia comes after insulin resistance. The truth is that recent data suggests that insulin resistance can follow hyperinsulinemia and vice versa. Obesity is commonly associated with insulin resistance and hyperinsulinemia, but although some molecular mechanisms have been proposed, there is no clear evidence as to which condition occur before in humans. Despite much controversy over the timing of the onset of hyperinsulinemia in obesity, it is well established that the presence of insulin is necessary for obesity to occur and that chronically elevated insulin levels enhance diet-induced obesity. Therefore, the aim of this review is to provide a comprehensive up-to-date on the molecular mechanisms underlying hyperinsulinemia and the relationship between hyperinsulinemia and insulin resistance in obesity. In addition, we will examine the role hyperinsulinemia plays in cellular senescence, cancer and in dysregulating the insulin/IGF-1/GH axis. Finally, we will discuss possible current therapeutic strategies targeting hyperinsulinemia that are being used to treat obesity-associated insulin resistance, including current pharmacological therapies, the effects of multiple dietary interventions, physical exercise, and surgery. We conclude that hyperinsulinemia is a prevalent condition in obesity, but its time of occurrence and relationship with obesity are still under investigation. Dietary interventions, particularly low glycemic load diets and low carbohydrate diets, as well as regular exercise have shown promise in reducing hyperinsulinemia, while the long-term efficacy and potential side effects of pharmacological interventions require further study.[cat] L'obesitat associada a la resistència a la insulina i la hiperinsulinemia són dues condicions de salut interrelacionades que han esdevingut cada vegada més prevalents en els últims anys. Durant molts anys, s'ha pensat que la hiperinsulinèmia ve després de la resistència a la insulina. La veritat és que les dades recents suggereixen que la resistència a la insulina pot seguir la hiperinsulinèmia i viceversa. L'obesitat s'associa comunament amb la resistència a la insulina i la hiperinsulinèmia, però tot i que s'han proposat alguns mecanismes moleculars, no hi ha evidència clara de quina condició ocorre abans en els éssers humans. Malgrat molta controvèrsia sobre el moment de l'aparició de la hiperinsulinèmia en l'obesitat, està ben establert que la presència d'insulina és necessària perquè es produeixi l'obesitat i que els nivells d'insulina crònicament elevats promouen l'obesitat induïda per la dieta. Per tant, l'objectiu d'aquesta revisió és proporcionar una actualització completa dels mecanismes moleculars subjacents a la hiperinsulinèmia i la relació entre la hiperinsulinèmia i la resistència a la insulina en l’obesitat. A més a més, examinarem el paper de la hiperinsulinèmia en la senescència cel·lular, el càncer i en la desregulació de l'eix insulina/IGF-1/GH. Finalment, es discutiran possibles estratègies terapèutiques actuals dirigides a la hiperinsulinemia que s'estan utilitzant per tractar l'obesitat associada a la resistència a la insulina, incloent les teràpies farmacològiques actuals, els efectes de múltiples intervencions dietètiques, l'exercici físic i la cirurgia. Concloem que la hiperinsulinèmia és una condició prevalent en l'obesitat, però el seu inici i relació amb l'obesitat encara estan en investigació. Les intervencions dietètiques, en particular les dietes de baixa càrrega glucèmica i dietes baixes en carbohidrats, a més de l'exercici regular, han demostrat ser prometedores per reduir la hiperinsulinèmia, mentre que l'eficàcia a llarg termini i els possibles efectes secundaris de les intervencions farmacològiques requereixen un estudi addicional

    European guideline on obesity care in patients with gastrointestinal and liver diseases - Joint ESPEN/UEG guideline

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    BACKGROUND: Patients with chronic gastrointestinal (GI) disease such as inflammatory bowel disease (IBD), irritable bowel syndrome (IBS), celiac disease, gastroesophageal reflux disease (GERD), pancreatitis, and chronic liver disease (CLD) often suffer from obesity because of coincidence (IBD, IBS, celiac disease) or related pathophysiology (GERD, pancreatitis and CLD). It is unclear if such patients need a particular diagnostic and treatment that differs from the needs of lean GI patients. The present guideline addresses this question according to current knowledge and evidence. OBJECTIVE: The objective of the guideline is to give advice to all professionals working in the field of gastroenterology care including physicians, surgeons, dietitians and others how to handle patients with GI disease and obesity. METHODS: The present guideline was developed according to the standard operating procedure for ESPEN guidelines, following the Scottish Intercollegiate Guidelines Network (SIGN) grading system (A, B, 0, and good practice point (GPP)). The procedure included an online voting (Delphi) and a final consensus conference. RESULTS: In 100 recommendations (3x A, 33x B, 24x 0, 40x GPP, all with a consensus grade of 90% or more) care of GI patients with obesity - including sarcopenic obesity - is addressed in a multidisciplinary way. A particular emphasis is on CLD, especially fatty liver disease, since such diseases are closely related to obesity, whereas liver cirrhosis is rather associated with sarcopenic obesity. A special chapter is dedicated to obesity care in patients undergoing bariatric surgery. The guideline focuses on adults, not on children, for whom data are scarce. Whether some of the recommendations apply to children must be left to the judgment of the experienced pediatrician. CONCLUSION: The present guideline offers for the first time evidence-based advice how to care for patients with chronic GI diseases and concomitant obesity, an increasingly frequent constellation in clinical practice

    European guideline on obesity care in patients with gastrointestinal and liver diseases - Joint European Society for Clinical Nutrition and Metabolism / United European Gastroenterology guideline

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    Background Patients with chronic gastrointestinal (GI) disease such as inflammatory bowel disease (IBD), irritable bowel syndrome (IBS), celiac disease, gastroesophageal reflux disease (GERD), pancreatitis, and chronic liver disease (CLD) often suffer from obesity because of coincidence (IBD, IBS, celiac disease) or related pathophysiology (GERD, pancreatitis and CLD). It is unclear if such patients need a particular diagnostic and treatment that differs from the needs of lean GI patients. The present guideline addresses this question according to current knowledge and evidence. Objective The objective of the guideline is to give advice to all professionals working in the field of gastroenterology care including physicians, surgeons, dietitians and others how to handle patients with GI disease and obesity. Methods The present guideline was developed according to the standard operating procedure for European Society for Clinical Nutrition and Metabolism guidelines, following the Scottish Intercollegiate Guidelines Network grading system (A, B, 0, and good practice point [GPP]). The procedure included an online voting (Delphi) and a final consensus conference. Results In 100 recommendations (3x A, 33x B, 24x 0, 40x GPP, all with a consensus grade of 90% or more) care of GI patients with obesity - including sarcopenic obesity - is addressed in a multidisciplinary way. A particular emphasis is on CLD, especially fatty liver disease, since such diseases are closely related to obesity, whereas liver cirrhosis is rather associated with sarcopenic obesity. A special chapter is dedicated to obesity care in patients undergoing bariatric surgery. The guideline focuses on adults, not on children, for whom data are scarce. Whether some of the recommendations apply to children must be left to the judgment of the experienced pediatrician. Conclusion The present guideline offers for the first time evidence-based advice how to care for patients with chronic GI diseases and concomitant obesity, an increasingly frequent constellation in clinical practice

    Abstracts of 51st EASD Annual Meeting

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    Background and aims: Presence and frequency of beta cell (BC) dysfunction(BCD) and insulin resistance (IR) in patients with newly diagnosedtype 2 diabetes mellitus (NDT2D) are imperfectly known, becauseprevious studies used small cohorts and/or only surrogate indexes of BCfunction and IR.We sought to assess BC function and IR with state-of-artmethods in the VNDS.Materials and methods: In 712 GADA-negative, drug naïve, consecutiveItalian NDT2D patients we assessed: 1. standard parameters; 2. insulinsensitivity (IS) by the euglycaemic insulin clamp); 3. BC functionby state-of-art modeling of prolonged (5 hours) OGTT-derived glucose/C-peptide curves. Thresholds for BCD and IR were the 25th percentilesof BC function and IS assessed with the same methods of the VNDS inItalian subjects with normal glucose regulation of the GENFIEV (n=340)and GISIR (n=386) studies, respectively.Results: In the VNDS, 89.8% [95% C.I.: 87.6 - 92.0%] and87.8% [85.4 - 90.2] patients had BCD and IR, respectively. Patientswith only one defect were 19.7% [16.8 - 22.6]. IsolatedBCD and isolated IR were present in 10.9% [8.6 - 13.2] and8.9% [6.8 - 11.0] patients, respectively. Coexistence of BCDand IR was observed in 78.9% [75.9 - 81.9] of the patients.1.4% [0.5 - 2.3] of the patients had no detectable alterations inBC function and IS. Patients (19.7%) with only one metabolicdefect had lower BMI, fasting glucose, HbA1c, triglycerides andBC function, and higher HDL-cholesterol and IS than patientswith both BCD and IR (p<0.01 or less after Bonferroni’scorrection).Conclusion: In conclusion, in NDT2DM patients: 1. at least 75.9% haveboth BCD and IR; 2. At least 87.6% and 85.4% have BCD and IR,respectively; 3. At least 16.8% have only one defect and a significantlydifferent (milder) metabolic phenotype compared to patients with bothdefects. These findings may be relevant to therapeutic strategies centeredon the metabolic phenotype of the patient.Clinical Trial Registration Number: NCT00879801; NCT01526720Supported by: University of Veron

    Molecular Mechanism of Congenital Heart Disease and Pulmonary Hypertension

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    This open access book focuses on the molecular mechanism of congenital heart disease and pulmonary hypertension, offering new insights into the development of pulmonary circulation and the ductus arteriosus. It describes in detail the molecular mechanisms involved in the development and morphogenesis of the heart, lungs and ductus arteriosus, covering a range of topics such as gene functions, growth factors, transcription factors and cellular interactions, as well as stem cell engineering technologies. The book also presents recent advances in our understanding of the molecular mechanism of lung development, pulmonary hypertension and molecular regulation of the ductus arteriosus. As such, it is an ideal resource for physicians, scientists and investigators interested in the latest findings on the origins of congenital heart disease and potential future therapies involving pulmonary circulation/hypertension and the ductus arteriosus
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