Prevalencia de hiperinsulinismo patológico post carga de glucosa y su relación con factores de riesgo cardiovascular, en adultos no diabéticos con insulinemia basal normal / Prevalence of pathologic hyperinsulinism after a glucose load charge: its relation to cardiovascular risk factors

Introducción: 25% de personas con hiperinsulinismo desarrolla diabetes 3-5 años luego del primer diagnóstico y 70% lo hará en el resto de la vida. Intervenir los niveles de glicemia desde que se detecta hiperinsulinemia evita la progresión a diabetes y restaura el metabolismo glicémico. Objetivos: Determinar la prevalencia de hiperinsulinismo patológico post-carga de glucosa (HPPG) y su relación con factores de riesgo cardiovascular en adultos 100 UI/ml a las 2 horas), sexo, hipertensión arterial, dislipidemia, malnutrición por exceso, sedentarismo, tabaquismo, ateromatosis e infarto miocárdico documentado. Con STATA 17 se calculó la prevalencia de variables en población general y según categoría de HPPG y se evaluó la significancia con prueba exacta de Fisher. Se compararon medias con ANOVA y t-test con nivel de significancia <0,05. Se usó regresión binomial para estimar Razón de Prevalencia e intervalos de confianza en variables cuantitativas y cualitativas. Resultados: la prevalencia de HPPG fue 41%. La edad promedio 37,5 años, el sexo masculino 52,9%, la hipertensión-arterial 40,5% y la dislipidemia 74,4%. Al comparar las poblaciones con y sin HPPG existieron diferencia estadísticamente significativa en las variables dislipidemia, hipertensión-arterial, malnutrición por exceso y sexo-masculino. La razón de prevalencia alcanzó a un 62%, 37%, 59% y 20% respectivamente. Conclusión: Se encontró una alta prevalencia de HPPG. Los factores de riesgo asociados a ella fueron dislipidemia, hipertensión arterial, malnutrición por exceso y sexo masculino. Esto sugiere que encontrar HPPG puede ser de utilidad para detectar precozmente a la población con un mayor riesgo de enfermedad cardiovascular.

Introduction: 25% of people with hyperinsulinism develop diabetes 3-5 years after the first diagnosis and 70% will do so in the rest of their lives. To control glycemia levels as soon as hyperinsulinemia is detected, progression to diabetes is prevented and glycemic metabolism is restored. Aim: To determine the prevalence of post-glucose load pathological hyperinsulinism (HPPG) and its relationship with cardiovascular risk factors in adults 100 uIU/ ml at 2 hours), sex, hypertension, dyslipidemia, excess malnutrition due to, sedentary lifestyle, smoking, documented atheromatosis and myocardial infarction. The prevalence of variables in the general population was calculated and, in relation to the HPPG category, significance is evaluated with Fisher's exact test. Finally means are compared with ANOVA and t-test. With significance level <0.05. Binomial regression was used to estimate the prevalence ratio and confidence intervals in quantitative and qualitative variables. Statistical analysis was performed with the STATA 17 software. Results: HPPG prevalence was 41%, mean age 37.5 years, male sex 52.9%, arterial hypertension 40.5% and dyslipidemia 74.4%. Un relation to the presence of HPPG a statistically significant difference in the variables dyslipidemia, arterial hypertension, malnutrition due to excess and male sex was found. The prevalence ratios were 62%, 37%, 59% and 20%, respectively. Conclusion: A high prevalence of HPPG was found. Risk factors associated to HPPG were dyslipidemia, arterial hypertension, malnutrition due to excess and male sex. Thus, HPPG can play a role in the early detection of a higher risk of cardiovascular disease in the general population.

Hyperinsulinemia and hyperglycemia: risk factors for recurrence of benign paroxysmal positional vertigo / Hiperinsulinismo e hiperglicemia: fatores de risco para recorrência de vertigem postural paroxística benigna

INTRODUCTION: Changes in carbohydrate metabolism may lead to recurrence of benign paroxysmal positional vertigo.OBJECTIVE: To evaluate the influence of the disturbance of carbohydrate metabolism in the recurrence of idiopathic BPPV.METHODS: A longitudinal prospective study of a cohort, with 41 months follow-up. We analyzed the results of 72 glucose-insulin curves in patients with recurrence of BPPV. The curves were classified into intolerance, hyperinsulinemia, hyperglycemia and normal.RESULTS: The RR for hyperinsulinism was 4.66 and p = 0.0015. Existing hyperglycemia showed an RR = 2.47, with p = 0.0123. Glucose intolerance had a RR of 0.63, with p = 0.096. When the examination was within normal limits, the result was RR = 0.2225 and p = 0.030.DISCUSSION: Metabolic changes can cause dizziness and vertigo and are very common in people who have cochleovestibular disorders. However, few studies discuss the relationship between idiopathic BPPV and alterations in carbohydrate metabolism. In the present study, we found that both hyperglycemia and hyperinsulinemia are risk factors for the recurrence of BPPV, whereas a normal test was considered a protective factor; all these were statistically significant. Glucose intolerance that was already present was not statistically significant in the group evaluated.CONCLUSION: Hyperinsulinemia and hyperglycemia are risk factors for the recurrence of idiopathic BPPV and a normal exam is considered a protective factor.

INTRODUÇÃO: As alterações do metabolismo do carboidrato podem levar a recorrência de vertigem posicional paroxística benigna.OBJETIVO: Avaliar a influência dos distúrbios do carboidrato na recorrência da VPPB idiopática.MÉTODO: Estudo longitudinal, do tipo coorte, prospectivo, com 41 meses de acompanhamento. Analisaram-se 72 resultados de curvas glicoinsulinêmicas em pacientes portadores de recorrência de VPPB. As curvas foram classificadas em intolerância, hiperinsulinemia, hiperglicemia e normal.RESULTADOS: O hiperinsulinismo teve RR = 4,66 e p = 0,0015. A hiperglicemia apresentou um RR = 2,47 e p = 0,0123. Na intolerância a glicose o RR = 0,63 e p = 0,096. No exame normal, o RR = 0,2225 e p = 0,030.DISCUSSÃO: As alterações metabólicas podem causar tontura e vertigem e são muito frequentes na população que apresenta distúrbios cocleovestibulares. Contudo, poucos trabalhos falam sobre a relação entre a VPPB idiopática e as alterações nos carboidratos. No presente estudo, verificou-se que tanto a hiperglicemia, quanto o hiperinsulinismo são fatores de risco para recorrência de VPPB, ao passo que o exame normal foi considerado fator protetor, todos estes estatisticamente significantes. Já a intolerância à glicose não teve significância estatística no grupo avaliado.CONCLUSÃO: O hiperinsulinismo e a hiperglicemia se comportam como fatores de risco para a recorrência de VPPB idiopática, assim como o exame normal como um fator protetor.

Obesity, insulin resistance and comorbidities ? Mechanisms of association / Obesidade, resistência à insulina e comorbidades ? Mecanismos de associação

Overall excess of fat, usually defined by the body mass index, is associated with metabolic (e.g. glucose intolerance, type 2 diabetes mellitus (T2DM), dyslipidemia) and non-metabolic disorders (e.g. neoplasias, polycystic ovary syndrome, non-alcoholic fat liver disease, glomerulopathy, bone fragility etc.). However, more than its total amount, the distribution of adipose tissue throughout the body is a better predictor of the risk to the development of those disorders. Fat accumulation in the abdominal area and in non-adipose tissue (ectopic fat), for example, is associated with increased risk to develop metabolic and non-metabolic derangements. On the other hand, observations suggest that individuals who present peripheral adiposity, characterized by large hip and thigh circumferences, have better glucose tolerance, reduced incidence of T2DM and of metabolic syndrome. Insulin resistance (IR) is one of the main culprits in the association between obesity, particularly visceral, and metabolic as well as non-metabolic diseases. In this review we will highlight the current pathophysiological and molecular mechanisms possibly involved in the link between increased VAT, ectopic fat, IR and comorbidities. We will also provide some insights in the identification of these abnormalities. Arq Bras Endocrinol Metab. 2014;58(6):600-9.

Excesso de gordura, geralmente definido pelo índice de massa corporal, está associado a distúrbios metabólicos (p. ex., intolerância à glicose, diabetes melito tipo 2 (DM2), dislipidemia) e não metabólicos (p. ex., neoplasias, síndrome dos ovários policísticos, esteatose hepática não alcoólica, glomerulopatia, fragilidade óssea etc.). No entanto, mais do que sua quantidade total, a forma da distribuição corporal de tecido adiposo constitui-se em um melhor indicador de risco para o desenvolvimento de tais doenças. O acúmulo de gordura na região abdominal e em tecido não adiposo (gordura ectópica), por exemplo, está associado ao aumento de risco para distúrbios metabólicos e não metabólicos. Por outro lado, observações sugerem que os indivíduos que apresentam adiposidade periférica, caracterizada por aumento das circunferências dos quadris e da coxas, têm melhor tolerância à glicose, redução das incidências de DM2 e da síndrome metabólica. Uma das alterações subjacentes na relação entre a obesidade, particularmente a visceral, e os distúrbios citados é a resistência à insulina. Nesta revisão, enfatizaremos os mecanismos fisiopatológicos e moleculares possivelmente implicados na ligação entre o aumento das gorduras visceral e ectópica, IR e comorbidades. Também mencionaremos os métodos diagnósticos mais frequentemente usados na identificação dessas anormalidades. Arq Bras Endocrinol Metab. 2014;58(6):600-9.

Hyperinsulinemia and its association with polycystic ovarian syndrome

To determine the variable clinical presentation of Poly cystic ovarian Syndrome [PCOS] and its association with Hyperinsulinaemia in young adolescent girls. A descriptive study was conducted for one year from February 2009-2010 at Isra University Hospital Hyderabad [IUH]. 136 adolescent girls who came in OPD with suspected features of polycystic ovarian syndrome were recruited. Biochemical test, ultrasound of pelvis and test to determine hyperinsulinemia were done .woman having preexisting ovarian pathology were excluded. All results were analyzed on statistical software SPSS version 16. Frequencies and percentages were calculated. Result: Insulin resistance significantly increased [43.4%] in girls who have shown the features of PCOS. Weight gain observed in 69 [50.7% - Obese] and 40[29.4%- very obese] of girls respectively. Different types of menstrual irregularities such as oligomenorrhea 50[36.8%], secondary amenorrhea 28 [20.6%] primary amenorrhea 5 [3.7%] were observed. 53[39.0%] adolescent girls had normal cycle but evidence of PCO on ultrasound. Infertility was found in 32 [23.5%] of participant followed by hirsutism and acne in 59 [43.4%] 45 [33.1%] of woman respectively. There is significant association of PCOS with hyperinsulinemia. Hyperinsulinemia if persist can lead to metabolic syndrome with its serious sequelae .Steps should be taken for early recognition of PCOS in young woman

Alteraciones metabólicas en hijos de padres con hipertensión arterial / Metabolic abnormalities in young offsprings of parents with essential hypertension

El antecedente familiar de hipertensión arterial en jóvenes sanos se ha asociado a hiperinsulinemia, que a su vez produciría aumento en el cortisol sérico, confluyendo ambos mecanismos en daño endotelial renal con la presencia de microalbuminuria. El objetivo del estudio consistió en evaluar en jóvenes sanos, hijos de hipertensos, la asociación entre los niveles de insulinemia, cortisol sérico y microalbuminuria, debido a su relación con mayor riesgo cardiovascular. Se realizó un trabajo transeccional y correlacional en la ciudad de Santa Fe, incluyendo 145 jóvenes sanos mayores de 18 años de edad, que se asignaron a dos grupos: aquellos con antecedente de primer grado de hipertensión arterial esencial (grupo de estudio) y sin dicho antecedente (grupo control). Se valoraron las concentraciones séricas en ayunas de insulina, cortisol, y los niveles de microalbuminuria en primera orina matutina. La media de edad fue de 20 ± 2.9 años, siendo el 58% mujeres. El grupo de estudio incluyó el 48% (n = 69). El 4.8% presentó insulino-resistencia, 13.8% microalbuminuria y el 52% hipercortisolinemia, no encontrándose diferencias significativas de los niveles séricos de insulina y cortisol, ni de microalbuminuria entre los grupos, así como tampoco correlación entre estas variables. No se encontró asociación entre el antecedente de 1er grado de hipertensión arterial y alteraciones de la homeostasis de insulina o cortisol así como tampoco evidencia de daño endotelial con presencia de microalbuminuria.

The familiar history of hypertension in healthy young offsprings is associated with hyperinsulinemia, which could lead to increased serum cortisol, resulting in renal endothelial damage and the presence of microalbuminuria. The aim of this study was to evaluate, in healthy young offsprings of hypertensive parents, association between insulin levels, serum cortisol and microalbuminuria attending to its relationship with increased cardiovascular risk. We performed a cross-sectional correlational study in Santa Fe, Argentina, including 145 healthy individuals aged over 18 years, allocated to two groups: those with a history of essential hypertensive parents (study group) and those without such history (control group). We evaluated fasting serum insulin, cortisol, and microalbuminuria levels in the first morning urine. The mean age was 20 ± 2.9 years, and 58% were women. The study group included 48% (n = 69) of the sample. 4.8% had insulin resistance, microalbuminuria 13.8% and 52% hipercortisolinemia, with no significant differences in serum insulin, cortisol, or microalbuminuria between groups. No correlation was found between these variables. In this study there was no association between a history of first degree hypertension and impaired insulin or cortisol homoeostasis.

[Congenital Hyperinsulinism: review of 12 Tunisian cases]

Congenital hyperinsulinism in infancy [CHI] is a heterogeneous disorder with respect to genetics and response to therapy. Data on CHI are sporadic in North African population. To characterize the clinical features and outcome of 12 Tunisian patients with CHI. data of patients diagnosed with CHI during the period 1989-2007 were retrospectively analyzed. Diagnosis was considered whenever hyperinsulinemia 10 UI/ml was concomitant to hypoglycemia<3mmol/l and/or high insulin to glucose ratio>0.3 and/or positif glucagon test. Transient causes of hypoglycemia, adrenal and growth hormone deficiency were excluded. There were nine infants diagnosed at a median age of 17 months and three newborns. Permanent hyperammoniemia, found in one patient, guided to leucine-sensitive hyperinsulinism. Seven patients presented with seizures, two with psychomotor delay and one with recurrent malaises. Among 42 assays of plasmatic insulin, when in hypoglycemia, 40% only were 10 U/ml. Three patients resisted to diazoxide and underwent subtotal pancreatectomy complicated by diabetes mellitus in two cases and persistent hypoglycemia in one patient. Histological examination concluded to diffuse hyperplasia of pancreatic cells. Diazoxide was discontinued in four out the eight responders patients. Four patients died, seven patients developed variable degrees of mental retardation and five suffered from epilepsy. Early onset forms were, as reported in the literature, mostly resistant to medical therapy. The high proportion of neurological sequelae is related to diagnosis delay or to a late surgery. We focus on the importance of a precocious diagnosis and aggressive treatment of hypoglycemia

Hipoglicemia infantil / Hypoglycemia of infancy

Hypoglycemia of infancy is a common metabolic disorder that can have serious neurological consequences. Therefore, its early diagnosis and treatment are crucial prognostic factors. Hypoglycemia has a variety of causes and a good clinical history, physical examination and laboratory determination will orient the correct diagnosis. Occasionally a molecular study will be required.

Alterations in cochlear function during induced acute hyperinsulinemia in an animal model / Alterações na função coclear durante a indução aguda de hiperinsulinismo em um modelo animal

Hyperinsulinism secondary to peripheral insulin resistance has been described as the most frequent etiologic factor in cochlear and vestibular syndromes. AIM: This experimental study recorded and analyzed evoked auditory potential changes using transtympanic electrocochleography (EcochG) during induced acute hyperinsulinism in an animal model. MATERIALS AND METHODS: Six adult male sheep were randomly divided into 2 groups. The animals were submitted to EcochG under general anesthesia, and a peripheral blood sample was collected to measure glycemia and insulinemia. Animals in the intervention group (n=3) received regular human insulin IV (0.1 U/kg). The control group (n=3) received saline solution. Glycemia and insulinemia were measured simultaneously with the recording of evoked potentials at 10-minute intervals during 90 minutes. RESULTS: The intervention group experienced a progressive suppression in action potential amplitude when compared to the control group (p=0.001). CONCLUSION: Data strongly suggest that acute induced hyperinsulinism suppresses cochlear function. Results may be attributed to loss of Na+K+ATPase activity in the stria vascularis, leading to loss of endocochlear potential and subsequent depolarization of cochlear hair cells as well as of neural cells in the auditory portion of cranial nerve VIII.

O hiperinsulinismo secundário à resistência periférica à insulina tem sido apontado como o fator etiológico mais frequente de síndromes tanto vestibulares como cocleares. OBJETIVO: Este estudo experimental registrou e analisou as alterações dos potenciais evocados auditivos através da eletrococleografia (ECoG) transtimpânica durante o hiperinsulinismo agudo induzido em um modelo animal. MATERIAL E MÉTODO: 6 ovelhas macho adultas foram divididas randomicamente em 2 grupos. Os animais submeteram-se ao exame de ECoG sob anestesia geral, e sangue periférico foi coletado para determinação de glicemia e hiperinsulinemia. Os animais do grupo intervenção (n=3) receberam insulina regular humana IV (0.1U/kG). O grupo controle (n=3) recebeu solução salina. Glicemia e insulinemia foram determinadas simultaneamente com o registro dos potenciais evocados a intervalos de 10 minutos, durante 90 minutos. RESULTADO: O grupo intervenção apresentou uma progressiva supressão da amplitude do potencial de ação quando comparado ao grupo controle (p=0.001). CONCLUSÃO: Os dados sugerem fortemente que o hiperinsulinismo agudo induzido suprime a atividade coclear. Os resultados podem ser atribuídos à perda da atividade da enzima Na+K+ATPase na estria vascular, levando à perda do potencial endococlear e da despolarização subsequente das células ciliadas assim como das células neurais que compõem a porção auditiva do VIII par craniano.

Insulino resistencia y síndrome metabólico en pacientes con enfermedad coronaria definida por angiografía / Insulin-resistance and metabolic syndrome in patients with coronary heart disease defined by angiography

Se examinó la frecuencia de insulino-resistencia (IR) y síndrome metabólico (SM) en pacientes coronarios empleando diferentes criterios de definición y se analizó cuáles mostraban mejor asociación con la presencia y gravedad de la afección. Fue un estudio casos-controles en 100 pacientes con edades entre 40 y 70 años que concurrieron a un centro hospitalario para realizarse una angiografía. IR fue definido por insulina >15 mU/l, el modelo hemostático de insulino-resistencia (HOMA-IR) >3.1 y la combinación del índice de masa corporal (IMC) >27.5 kg/m² con HOMA-IR >3.6. SM fue definido según International Diabetes Federation y American Heart Association / National Heart, Lung, and Blood. Insulina >15 mU/l y HOMA-IR >3.1 tuvieron la misma sensibilidad, (60.3%), y se asociaron significativamente con la extensión de la enfermedad coronaria, p = 0.001 y p = 0.009 respectivamente. En cambio, IMC >27.5 kg/m² con HOMA-IR >3.6 mostró menor sensibilidad, (43.1%), y menor asociación con la gravedad, (p = 0.028). Los odds ratio (OR) para enfermedad coronaria fueron respectivamente: 3.16 (IC 95% 1.28-7.79), p = 0.012; 2.93 (IC 95% 1.20-7.19) p = 0.019; 2.86 (IC 95% 1.10-7.41), P = 0.031. La frecuencia de SM definida según American Heart Association / National Heart, Lung, and Blood fue mayor en coronarios versus controles (62.1% versus 33.3%, p = 0.003), se asoció con la enfermedad en uno o en múltiples vasos (p = 0.011) y fue su predictor, OR = 4.22 (IC 95% 1.65-10.83) p = 0.003. Sin embargo, SM definido según International Diabetes Federation no se asoció con la presencia ni con la gravedad de la enfermedad.

The frequency of insulin-resistance (IR) and metabolic syndrome (MS) were examined in coronary patients using different criteria of definition. It was also analyzed which of them indicated a strong association with the presence and severity of the disease. This was a case-control study on 100 patients between 40 and 70 years old, assisted in a hospital center and there examined by angiography. IR was defined by insulin >15 mU/l, Homeostatic Model Assessment for insulin-resistance (HOMA-IR) >3.1 and the combination body mass index (BMI) >27.5 kg/m² with HOMA-IR >3.6. MS was defined according to International Diabetes Federation and American Heart Association/National Heart, Lung and Blood Institute. Insulin >15 mU/l and HOMA-IR >3.1 had similar sensibility, 60.3%, and were significantly associated with the extension of coronary heart disease, p = 0.001 and p = 0.009 respectively. Whereas, BMI>27.5 kg/m² with HOMA-IR>3.6 showed a lower sensibility, 43.1% and less association with severity, p = 0.028. The odds ratio (OR) for coronary heart disease were respectively: 3.16 (CI 95 1.28-7.79), p = 0.012; 2.93 (CI 95% 1.20-7.19) p = 0.019; 2.86 (CI 95% 1.10- 7.41), p = 0.031. The frequency of SM defined according to American Heart Association/National Heart, Lung and Blood Institute was higher in coronary patients vs. controls (62.1% vs. 33.3%, p = 0.003). It was associated with disease in one or more vases (p = 0.011) and was its predictor, OR = 4.22 (CI 95% 1.65-10.83) p = 0.003. However, SM defined according to International Diabetes Federation was not associated with the presence or severity of coronary heart disease.

La macrosomía en el embarazo complicado con diabetes / Macrosomia in pregnancy complicated by diabetes

La macrosomía neonatal es la complicación más frecuente que sufre el hijo de madre diabética y su presencia se asocia con un importante aumento de la morbimortalidad perinatal. El responsable principal de su aparición es el hiperinsulinismo fetal que aparece como respuesta a la hiperglucemia fetal, la cual es consecuencia de la hiperglucemia materna. El diagnóstico prenatal de esta alteración se hace en la actualidad por medio de la ecografía fetal, la cual permite calcular el peso del feto con bastante exactitud...

Síndrome dos ovários policísticos e insulina: revisão do vínculo fisiopatológico e do tratamento com sensibilizadores de insulina / Polycistic ovary syndrome and insulin: revision of entail physiopathologic and insulin sensitizing agents treatment

A síndrome dos ovários policísticos (SOP) é uma desordem complexa que engloba um amplo espectro de sinais e sintomas, predominando aqueles de disfunção ovariana. Acomete cerca de 10 por cento das mulheres em idade reprodutiva. Resistência insulínica e hiperinsulinemia desempenham papel importante na patogênese da doença. Nesse contexto, a utilização de sensibilizadores de insulina (metformina e glitazonas) tem sido recentemente proposta como terapia de escolha para muitas mulheres com SOP. O uso desse agentes está associado a decréscimo nos níveis de androgênios e gonadotropinas, melhora na tolerência à glicose, perfil lipídico e função endotelial com redução dos marcadores de doença aterosclerótica subclínica. O tratamento é potencialmente útil no controle do hiperandrogenismo, das alterações metabólicas e particularmente da fertilidade.

Polycystic ovary syndrome is a complex disorder that encompasses a wide range of signs and symptoms, mainly those related with ovarian dysfunction, and affects about 10 per cent of women during their reproductive years. Insulin resistance and hyperinsulinemia play important role in the pathogenesis of the disease. So, insulin-sensitizing agents (metformin and glitazones) have been recently proposed as the therapy of choice for many women with polycystic ovary syndrome. Insulin sensitizer treatment has been associated with a reduction in serum androgen levels and gonadotropins, improvement in glucose tolerance, lipid profile and endothelial function with reduction in sub-clinica atherosclerotic markers. The treatment is potentially useful in the control of hyperandrogenism, metabolic changes and improvement of fertility.

Body fat distribution in childhood obesity: association with metabolic risk factors.

OBJECTIVES: To evaluate the clinical significance of body fat distribution in childhood obesity, we investigated the associations of subcutaneous and intraabdominal (preperitoneal and visceral) fat, estimated by ultrasonography, with metabolic risk factors. SUBJECTS: Fifty-one obese (age 11.5+/- 2.6 years) and 33 non-obese (age 12.2+/- 2.7 years) children. STUDY DESIGN: Case control study. METHODS: Ultrasonographic measurements of fat thickness [maximum and minimum preperitoneal fat thicknesses (Pmax, Pmin), maximum and minimum subcutaneous fat thicknesses (Smax, Smin), visceral fat thickness (V), triceps (Tr) and subscapular (Ss) skin fold thicknesses] were documented. Blood pressures, lipid profiles, fasting insulin levels, glucose/insulin ratio and HOMA IR (homeostasis model assessment for insulin resistance) were evaluated in both groups and these parameters were correlated with body fat distribution. RESULTS: In the obese group, fasting insulin level was correlated to Smin, Smax, and Pmin. HOMA, accordingly, was also correlated to Smin, Smax, and Pmin. Fasting insulin level and HOMA showed no correlation with either Pmax or visceral fat thickness. ANALYSIS: Abdominal subcutaneous fat thickness measurements were the best predictors of hyperinsulinemia (R2: 0.32). CONCLUSION: We did not observe a significant correlation between blood pressure, lipid parameters and body fat distribution in obese group. Abdominal subcutaneous fat thickness might be a better predictor of the risk for hyperinsulinemia in childhood obesity.

Hiperinsulinismo congénito: revisión de aspectos diagnósticos y terapéuticos a propósito de un caso clínico / Congenital hyperinsulinism: review of diagnostic and therapeutic

El hiperinsulinismo congénito (HC) es la causa más común de hipoglicemia persistente en el primer año de vida. Se acompaña de riesgo elevado de daño neurológico irreversible. En los últimos años se ha profundizado en el conocimiento sobre su patogenia, destacándose la heterogenicidad clínica, histológica y genética, con claras implicancias en el diagnóstico y tratamiento. Se describe el caso de un lactante portador de HC que debuta con hipoglicemias sintomáticas a los 5 meses de vida. El objetivo de esta comunicación es, a la luz de los conocimientos actuales, analizar los criterios diagnósticos y terapéuticos de esta patología. Se destaca la importancia de aplicar un algoritmo para guiar el estudio paraclínico y descartar las etiologías más frecuentes asociadas con la hipoglicemia.

Congenital hyperinsulinism (HC) is the most common etiology of persistent hypoglycemia in infants. It is associated with a high risk of irreversible neurological damage. Knowledge about its pathogenesis has improved in the past few years. It is characterized by a heterogeneous clinical presentation, histology and genetic which leads to special diagnosis and treatment features. This is a case report of a 5 month old with HC who had symptomatic hypoglycemia. The objective of this communication is to analyze the diagnosis and treatment criteria of HC. The need to follow a clinical and laboratory guideline for diagnosis will help exclude other causes of hypoglycemia.

Hyperinsulinemia and its potential role in preeclampsia

Pre-eclampsia remains one of the leading causes of maternal and fetal morbidity and mortality. Despite extensive researches, our knowledge of the etiology and pathphysiology of preeclampsia is still limited. Recently, insulin resistance is implicated in the pathogenesis of preeclampsia. We conducted a nested case-control study to test the hypothesis that insulin resistance is associated with preeclampsia. Blood glucose and insulin serum concentrations, both fasting and postprandial, were evaluated in sixty preeclamptic patients [thirty with mild preeclampsia and thirty with severe preeclampsia] and thirty normotensive control during the third trimester of gestation. Compared with control group, women who have preeclampsia had significantly higher serum insulin levels both fasting and postprandial, also it was found that the preeclamptic group patients with severe preeclampsia had significantly higher insulin serum levels compared to women with mild preeclampsia, No significant difference was observed between the three groups as regard to both fasting and postprandial blood glucose level

Impact of Visceral Fat on the Metabolic Syndrome and Nonalcoholic Fatty Liver Disease

Visceral fat has been reported to be associated with nonalcoholic fatty liver disease (NAFLD) and the metabolic syndrome (MetS). We assessed the prevalence of both NAFLD and the MetS, measured visceral fat thickness VFT), and estimated the physical activity indexes of 224 relatively healthy hospital workers. We also investigated the associations between both VFT and physical activity index and each of NAFLD and the MetS. The MetS was diagnosed according to the guidelines outlined by the Adult Treatment Panel III, and NAFLD was diagnosed by ultrasonography. Subjects with hepatitis B and C infections and those reporting moderate alcohol consumption were excluded from the study. The prevalence of the MetS was 11.6% and that of NAFLD was 41.5%. Many subjects with the MetS had NAFLD (73.1%), and some subjects with NAFLD (20.4%) also had several components of the MetS (p=0.001). VFT was significantly increased by both the addition of components of the MetS and the severity of NAFLD (p<0.001). In addition, VFT was independently associated with NAFLD (odds ratio [OR], 1.10; 95% confidence interval [CI], 1.02-1.19) in subjects with more than 2 components of the MetS. In contrast, habitual physical activity was reversely associated with NAFLD (OR, 0.29; 95% CI, 0.10-0.87). In conclusion, an increased visceral fat content and reduced physical activity could be not only biological markers but also therapeutic targets in the treatment of NAFLD and the MetS.

Relación entre hiperinsulinemia, disfunción diastólica e hipertrofia del ventrículo izquierdo en pacientes con hipertensión arterial sistémica / Association of hyperinsulinemia with left ventricular hypertrophy and diastolic dysfunction in patients with hypertension

Background: Hypertension is the main independent cardiovascular risk factor. However, there are additional factors that induce organic damage. Aim: To assess the association between hyperinsulinemia, ventricular hypertrophy and left ventricular diastolic function. Patients and Methods: Seventy-four patients aged 30 to 65 years, with mild or moderate systemic hypertension, with overweight or mild obesity and normal glucose tolerance curve (GTC), were studied. Serum insulin was measured during GTC. The maximum levels of insulin and glucose were observed 60 minutes after the oral glucose load and they were expressed as rG/1. Patients were stratified in three groups according to their glucose and insulin fasting levels (I0) and post-glucose challenge levels (rG/I): Group 1 (normoinsulinemic patients) I0 <17 mU/mL and rG/I >2 (2.45+0.4). Group 2 (post-prandial hyperinsulinemic patients) I0 <17 mU/mL and rG/I <2> 1 (1.34+0.3). Group 3 (persistently hyperinsulinemic patients) I0 >17 mU/mL and <1 (0.7+0.3). Left ventricular mass and its diastolic function were measured by Doppler echocardiography. Results: No differences in blood pressure or age were observed between groups. There was a negative correlation between ventricular mass and rG/1 (r =-0.282, p =0.015). Left ventricular diastolic dysfunction was significantly more deteriorated in group 3, as compared with group 1 (p <0.001 ANOVA). There was a significant correlation between g/GI and diastolic dysfunction (r =0.232 p =0.047). Conclusions: Fasting, post challenge hyperinsulinemia and a rG/I <1 are associated with higher ventricular mass and left ventricular diastolic dysfunction, independent of blood pressure and age.

Miocardiopatia diabética / Diabetic cardiomyopathy

A miocardiopatia diabética é uma doença do músculo cardíaco causada pelo diabetes mellitus e não relacionada às patologias vascular e valvular ou à hipertensão arterial sistêmica. Observações experimentais e clínicas têm demonstrado hipertrofia, necrose, apoptose e aumento do tecido intersticial miocárdico. Acredita-se que a miocardiopatia diabética seja decorrente de anormalidades metabólicas como hiperlipidemia, hiperinsulinemia e hiperglicemia, e de alterações do metabolismo cardíaco. Tais alterações podem causar aumento do estresse oxidativo, fibrose intersticial, perda celular e comprometimento do trânsito intracelular de íons e da homeostase do cálcio. Clinicamente, é possível a detecção de disfunção diastólica assintomática na fase inicial. No momento em que surgem os sinais e sintomas de insuficiência cardíaca, observamos disfunção diastólica isolada, sendo que o comprometimento da função sistólica, habitualmente, é tardio. O tratamento da miocardiopatia diabética com insuficiência cardíaca não difere das miocardiopatias de outras etiologias e deve seguir as diretrizes de acordo com o comprometimento da função ventricular, se diastólica isolada ou diastólica e sistólica.

Diabetic cardiomyopathy is a myocardial disease caused by diabetes mellitus unrelated to vascular and valvular pathology or systemic arterial hypertension. Clinical and experimental studies have shown that diabetes mellitus causes myocardial hypertrophy, necrosis, and apoptosis, and increases interstitial tissue. The pathophysiology of diabetic cardiomyopathy is incompletely understood. It appears that metabolic perturbations such as hyperlipidemia, hyperinsulinemia, hyperglycemia, and changes in cardiac metabolism are involved in cellular consequences leading to increased oxidative stress, interstitial fibrosis, myocyte death, and altered intracellular ions transient and calcium homeostasis. Clinically, an early detection of asymptomatic diastolic dysfunction is possible. When patients develop signals and symptoms of heart failure, isolated diastolic dysfunction is usually detected. Systolic dysfunction is a late finding. Treatment of heart failure due to diabetic cardiomyopathy is not different from myocardiopathies of other etiologies and must follow the guidelines according to ventricular function, whether diastolic or diastolic and systolic impairment.

Association between Insulin, Insulin Resistance, and Gallstone Disease in Korean General Population / 대한소화기학회지

BACKGROUND/AIMS: Diabetes is one of the risk factors of gallstone diseases. Many studies found a positive association between insulin and gallstones in individuals with diabetes. However, this association is unclear in non-diabetes. So we conducted a case-control study for the evaluation of the association between gallstone diseases and fasting serum insulin level, insulin resistance in non-diabetic Korean general population. METHODS: This study was a prospective case-control study on 118 Korean subjects which included clinical examination, abdominal ultrasound, and blood chemistries. Serum fasting insulin level were determined by radioimmunoassay and concentrations of cholesterol, glucose, and triglycerides by standard enzymatic colorimetric methods. Insulin resistance was determined by the homeostasis model assessment (HOMA-IR). Body mass index (BMI), percentage of body fat, and waist hip ratio were also measured. RESULTS: We studied 118 subjects with no clinical evidence of diabetes mellitus and serum glucose<126 mg/dL. Compared with controls (n=89), cases (n=29) had higher levels of serum insulin, glucose, triglyceride levels, and BMI. In t-test and chi-square test for variables, the association between gallstone disease and serum insulin, HOMA-IR index, and BMI were statistically significant (p<0.05). In multiple logistic regression analysis, gallstone disease risk increased with the level of serum insulin (p=0.024, odds ratio=1.376) and HOMA-IR index (p=0.013, odds ratio=2.006). CONCLUSIONS: We suggest that hyperinsulinemia and insulin resistance could be associated with gallstone formation in individuals without clinical diagnosis of diabetes mellitus and with normal serum glucose level.