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Query: UMLS:C0311277 (abdominal obesity)
 2,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent evidence suggests that non-insulin-dependent diabetes mellitus (NIDDM) and cardiovascular disease, rather than being related as underlying disease and complication, share common genetic and environmental antecedents, that is, they "spring from the same soil." Fetal and early-life nutritional deficiencies appear to predispose persons to both NIDDM and cardiovascular disease in later life. The insulin resistance syndrome, including abdominal obesity, may constitute the intermediate link between fetal and early-life nutritional deficiency and later disease. The insulin resistance syndrome includes insulin resistance, hyperinsulinemia, abdominal obesity, dyslipidemia with high triglyceride and low high-density lipoprotein cholesterol levels, and hypertension. Each element of the insulin resistance syndrome has been firmly established as a risk factor for development of diabetes. In addition, most of these elements are also well-recognized cardiovascular risk factors, although the weight of evidence now suggests that hyperinsulinemia itself is not. This last point is significant because of concern that aggressive insulinization of diabetic patients, which has been proved to reduce microvascular complications, might paradoxically increase the risk for large-vessel atherosclerosis. Available clinical trials suggest that this fear is unwarranted, but definitive trials are needed to resolve this important clinical question.
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PMID:Do non-insulin-dependent diabetes mellitus and cardiovascular disease share common antecedents? 855 1

Being overweight, especially in the abdominal region, is a risk factor for cardiovascular disease, the onset of diabetes in adults, stroke, and mortality. Malnutrition in utero or early childhood may lead to fatness later in life. The authors tested the hypothesis that poor linear growth during childhood predicts fatness and the high-risk fat patterning of young Guatemalan adults. Findings are based upon the analysis of prospectively collected data on 161 male and 372 female Guatemalans measured as children during 1969-77 and remeasured as adults in 1988-89 (men and women) and 1991-94 (women only). Childhood stunting was associated with a lower body mass index (BMI) and percent body fat in men, while no association was found in women. Both male and female severely stunted children had significantly greater adult abdominal fatness, after controlling for overall fatness and confounders. The adult waist:hip ratio was increased by 0.65 in men and 0.29 in women for each height-for-age z score less at age 3. Migration to urban centers was significantly associated with a greater waist:hip ratio in severely stunted females. In a subsample of 137 women, short and thin newborns had significantly greater adult abdominal fatness compared with long and thin or short and fat newborns or children who became stunted postnatally. The adult waist/hip ratio was increased by 1.58 for each kilogram less birth weight. Findings suggest that in countries where maternal and child malnutrition exist in the context of rapid economic development and urban migration, abdominal obesity and related chronic diseases are likely to increase.
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PMID:Infant and child growth and fatness and fat distribution in Guatemalan adults. 992 63

Undernutrition is a frequent complication of evolutive and chronic HIV (human immunodeficiency virus) infection characterized by bodyweight loss and changes in body composition. The Centers for Disease Control and Prevention define AIDS wasting as involuntary loss of more than 10% of body weight, plus more than 30 days of either diarrhea, or weakness and fever. Wasting syndrome has been considered as a case definition of the AIDS disease since 1987. Wasting syndrome is clearly linked to disease progression and death. Despite the progress under the era of highly active antiretroviral therapy (HAART), wasting is still a problem for people with AIDS. A small part of the weight lost is fat. More important is the loss of "lean body mass", which is mostly muscle. Body composition changes during HIV infection are different from those observed in food deprivation. Under the era of HAART, a HIV-associated adipose redistribution syndrome (HARS) was described that associates subcutaneous lipoatrophy and abdominal obesity linked to various metabolic disorders. Several factors contribute to wasting syndrome. Not only low food intake and poor nutrient absorption, but mainly altered metabolism (increased resting energy expenditure) and specific disturbances in protein turnover, which is also increased. Nutritional evaluation of HIV-infected patients should include the measurement of body composition and analysis of nutritional parameters, including albumin, transthyretin and C-reactive protein. Transthyretin seems to be particularly useful to follow the recovery period of malnutrition.
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PMID:Body composition and nutritional parameters in HIV and AIDS patients. 1255 39

The metabolic syndrome (MetS) is a huge public health problem worldwide, being one of the major causes of cardiovascular disease, responsible for a growing number of premature deaths throughout the world. MetS includes a cluster of anomalies, such as: abdominal obesity, insulin resistance, hyperinsulinemia, hypertension, type 2 diabetes mellitus or glucose intolerance, hypertriglyceridemia etc. The number of people with MetS increases with age, affecting more than 40% of people in their 60s and 70s. About 30% of European people over 50 have MetS. Some experts estimate that as many as two thirds of Americans may be suffering from MetS. The exact cause of MetS is not known: genetics play a minor role, acquired in-utero factors also play a role (prenatal malnutrition, toxin exposure, exposure to high levels of maternal cortisol). For most people, the MetS results primarily from lifestyle factors, such as: chronic stress, inadequate exercise. The MetS can be avoided and reversed in most cases. Weight loss is both a treatment and goal for MetS patients. Moderate weight loss, in the range of 5-10% of body weight, can help restore body's ability to recognize insulin and greatly reduce the chance that the syndrome will evolve into a more serious illness. In most people weight loss will lower blood pressure and improve triglyceride levels. Increased activity alone can improve insulin levels. Physical activity result in a weight loss, improved blood pressure, improved cholesterol and triglyceride level and reduced risk of developing diabetes. It is also important to treat: hyperlipidemia, hypertension, prothrombotic state.
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PMID:The metabolic syndrome--a multifaced disease. 1552 15

Drug abuse is associated with significant health risk. Whether drug abusers are at a higher risk of suffering the metabolic syndrome is not widely known. The metabolic syndrome is a cluster of metabolic abnormalities, including hyperinsulinemia, hypertension, dyslipidemia, and abdominal obesity, and is probably triggered by initial imbalances at the cellular level in various critical metabolic pathways. These initially small metabolic imbalances are believed to cascade with time and lead to larger problems. Some indications that drug abuse may increase the risk of the metabolic syndrome include the following: Drug-abusing patients have higher rates of diabetes complications. Substance abuse is a significant contributing factor for treatment noncompliance in diabetes. Nutrition education can enhance substance abuse treatment outcomes. Each type of drug/substance abuse has a unique profile of toxicity. For example, the amphetamines generally affect the cardiovascular and neurological systems, worsening the risk factors for the metabolic syndrome. Methamphetamine (meth) abusers suffer cognitive deficits and abnormal metabolic activity, which affect nutritional status. This condition is further worsened by a drastic reduction in oral health in meth abusers, resulting in improper chewing and, therefore, digestion. Nutritional deficiency in combination with drug abuse would increase the risk of developing the metabolic syndrome by increasing cell damage, augmenting excitotoxicity, reducing energy production, and lowering the antioxidant potential of the cells. Another potential risk factor in the development of the metabolic syndrome is genetic vulnerability, especially in combination with drug abuse and nutritional deficiencies. The strategies available to treat this problem include pharmacological agents as well as dietary antioxidants. Such measures may be useful in reducing drug abuse-related toxicity that may lead to the metabolic syndrome.
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PMID:Metabolic syndrome in drug abuse. 1807 64

Calorie intake is an important determinant of health. Excessive energy intake is associated with abdominal obesity, type 2 diabetes, cardiovascular disease, cancer, and premature mortality. Calorie restriction (CR) without malnutrition increases maximal lifespan by preventing many age-associated chronic diseases and by preserving function at more youthful-like states in rodents. In overweight and obese humans CR improves metabolic health and reduced mortality for type 2 diabetes, cardiovascular disease and cancer. In middle-aged healthy lean individuals CR causes many of the same cardiometabolic adaptations that occur in long-lived CR rodents, including decreased metabolic, inflammatory, and hormonal risk factors for diabetes, hypertension, cardiovascular disease and cancer Protein and polyphenols intake, and physical activity may have additional beneficial effects in preventing diseases and promoting health. Additional studies are needed to identify the precise calorie, protein and polyphenols intake and amount of exercise needed for optimal health in each individual, depending on his/her age, sex and genetic background.
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PMID:[Nutrition, adiposity and health]. 1827 33

Women are doubly vulnerable to malnutrition, because of their high nutritional requirements for pregnancy and lactation and also because of gender inequalities in poverty. Undernutrition and overnutrition coexist in developing countries undergoing rapid nutrition transition, and women are susceptible to this double burden of "dysnutrition," often cumulating stunting or micronutrient malnutrition with obesity or other nutrition-related chronic diseases. The purpose of the present paper is to describe the adverse impact of income and gender inequities on women's nutritional health, and the dramatic consequences, not only for women themselves, but for children, families, and societies. Improving women's resources, including health, nutrition, education, and decisional power, is critical for equity and for the health of children and adults of future generations, since poor fetal and infancy nutrition is another risk factor for chronic diseases, in particular abdominal obesity, type 2 diabetes, hypertension, and cardiovascular disease. Addressing malnutrition and nutrition-related chronic diseases simultaneously is a challenge facing developing countries, and examples of promising initiatives are provided. Focusing on women along the lifecycle, according to the continuum of care approach, is essential to achieving the Millennium Development Goals and to breaking the intergenerational cycle of poverty, malnutrition, and ill-health.
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PMID:Poverty: the double burden of malnutrition in mothers and the intergenerational impact. 1857 81

In view of the epidemic obesity in childhood, facing the disease and its associated morbidities early at this age becomes crucial for public health researchers and care givers. The present review focuses on pediatric Non Alcoholic Fatty Liver Disease (NAFLD) among co-morbidities, being the disease yet under diagnosed and under treated despite a prevalence growing exponentially. Evidences suggest that the environmental background for the development of NAFLD may be established in early life, and that the duration of the disease affects probably the likelihood of progression to more severe disease (necro-inflammation or Non Alcoholic SteatoHepatitis, also termed, NASH; fibrosis and cirrhosis). NAFLD associates with abdominal obesity, insulin resistance and features of metabolic syndrome. In genetically prone individuals, malnutrition (i.e., excessive consumption of saturated fats and refined sugars) leads to the derangement of the adipose tissue architecture and homeostasis, the peripheral and hepatic resistance to insulin-stimulated glucose uptake, thus favoring a condition of chronic low-grade inflammation. Excessive nutrients cannot be stored in the adipose tissue and overflow elsewhere, mainly to the muscle tissue and liver. Fat deposition in both sites enhances insulin resistance and further deposition of fats in a vicious manner. What is of special interest comparing NAFLD in children and adults is that the histological appearance of the disease differs significantly, likely representing a yet physiological response to environmental stressors in children and a long-term adaptation in adults. In this article, we review the current concepts about paediatric NAFLD, its pathogenesis, diagnosis and treatment, with particular regard to lifestyle and foods habits.
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PMID:Nonalcoholic fatty liver disease in children. 1915 26

Latin America is experiencing an epidemic of cardiovascular disease and type-2 diabetes mellitus. The rise in life-expectancy and increasingly rapid urbanization have resulted in a greater prevalence of overweight, obesity and metabolic syndrome. In Latin America, there is a high level of susceptibility to the development of insulin resistance and low-grade inflammation at relatively low levels of abdominal obesity. This susceptibility is associated with the adaptive response of the fetus to deficient fetal nutrition, which results in a loss of anatomical structures such as nephrons, cardiomyocytes and pancreatic beta cells. These adaptations may prove detrimental if food becomes abundant again after birth. In Latin America, the high prevalence of maternal and fetal malnutrition could mean that the resulting fetal adaptations may contribute to an increased risk of cardiometabolic disease. The socioeconomic differences that exist between developed and underdeveloped countries may be reflected in different biological adaptations, which could invalidate the diagnostic criteria and preventive and therapeutic approaches that have been recommended on the basis of research carried out in populations with different characteristics. Clinical studies are needed to evaluate the effectiveness of interventions recommended for preventing and aiding recovery from cardiometabolic disease in Latin America.
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PMID:Cardiometabolic disease in latin america: the role of fetal programming in response to maternal malnutrition. 1948 Jul 63

Neonatal malnutrition is associated with metabolic syndrome in adulthood. Maternal hypoprolactinaemia at the end of lactation (a precocious weaning model) caused obesity, leptin resistance and hypothyroidism in adult offspring, suggesting an association of prolactin (PRL) and programming of metabolic dysfunctions. Metabolic syndrome pathogenesis is still unclear, but abdominal obesity, higher triglycerides, lower high-density lipoprotein (HDL-c) and insulin resistance have been proposed to be important factors involved. We studied the consequences of maternal hypoprolactinaemia during lactation on parameters associated with metabolic syndrome. Lactating Wistar rats were treated with bromocriptine (BRO, 1 mg twice a day) or saline on days 19, 20 and 21 of lactation and their offspring were followed from weaning until 180 days old. Adult BRO offspring had higher body weight (+10%, P < 0.05), total body fat (+41%, P < 0.05), visceral fat (+20%, P < 0.05), subcutaneous fat (+3 times, P < 0.05) and total body protein (+24%, P < 0.05). BRO group presented hyperglycaemia (+16%, P < 0.05), lower muscle glycogen (51%, P < 0.05), higher cholesterol (+30%, P < 0.05), higher low-density lipoprotein (LDL-c) (+1.5 times, P < 0.05), higher triglycerides (+49%, P < 0.05), lower HDL-c (28%, P < 0.05), hyperleptinaemia (+2.9 times, P < 0.05), hypoadiponectinaemia (16%, P < 0.05) and hypoprolactinaemia (54%, P < 0.05) as well as higher insulin resistance index (+24%, P < 0.05). Regarding adrenal function, BRO rats showed hypercorticosteronaemia (+46%, P < 0.05) and higher total catecholamine (+37%, P < 0.05). In the hypothalamus, no change was observed in protein expression of the leptin signalling pathway. Thus, neonatal malnutrition induced by maternal PRL inhibition during late lactation programs for obesity, dyslipidaemia and insulin resistance in adult offspring increasing the risk for metabolic syndrome development.
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PMID:Maternal prolactin inhibition during lactation programs for metabolic syndrome in adult progeny. 1973 3


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