Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aging is associated with a number of physiologic and functional declines that can contribute to increased disability, frailty, and falls. Contributing factors are the loss of muscle mass and strength as age increases, a phenomenon called sarcopenia. Sarcopenia can result or be exacerbated by certain chronic conditions, and can also increase the burden of chronic disease. Current research has demonstrated that strength-training exercises have the ability to combat weakness and frailty and their debilitating consequences. Done regularly (e.g., 2 to 3 days per week), these exercises build muscle strength and muscle mass and preserve bone density, independence, and vitality with age. In addition, strength training also has the ability to reduce the risk of osteoporosis and the signs and symptoms of numerous chronic diseases such as heart disease, arthritis, and type 2 diabetes, while also improving sleep and reducing depression. This paper reviews the current research on strength training and older adults, evaluating exercise protocols in a variety of populations. It is clear that a variety of strength-training prescriptions from highly controlled laboratory-based to minimally supervised home-based programs have the ability to elicit meaningful health benefits in older adults. The key challenges as this field of exercise science moves forward are to best identify the most appropriate strength-training recommendations for older adults and to greatly increase the access to safe and effective programs in a variety of settings.
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PMID:The benefits of strength training for older adults. 1455 38

Amylin is a polypeptide hormone produced in pancreatic beta-cells that belongs to the family of calcitonin gene-related peptides. There is a 20% sequence homology between amylin and calcitonin and 44% homology with calcitonin gene-related peptide. Amylin and its fragments stimulate the proliferation of osteoblasts, inhibit bone resorption, and increase bone density and the amount of bone mass. We measured amylin total and unreduced amylin fasting plasma levels in patients with osteoporosis ( n=28; 3 men, 25 women; mean age 65 years), type 2 diabetes mellitus ( n=10; 5 men, 5 women; 64 years), and in the control group ( n=24; 11 men, 13 women; 53 years) using an ELISA kit with immunofluorescent detection (Linco). Amylin total plasma levels in patients with osteoporosis were 3.33+/-0.46 pmol/l (mean+/-SEM), in patients with type 2 diabetes 6.29+/-1.47 pmol/l (mean+/-SEM), and in the control group 8.48+/-3.12 pmol/l (mean+/-SEM). Mean plasma levels were lower in patients with osteoporosis than in patients with type 2 diabetes and in the control group. Unreduced amylin plasma levels in patients with osteoporosis ( n=28) were 2.51+/-0.87 pmol/l (mean+/-SEM), in patients with type 2 diabetes ( n=10) 4.15+/-0.95 pmol/l (mean+/-SEM) and in the control group ( n=5) 13.50+/-3.94 pmol/l (mean+/-SEM). Plasma levels were significantly lower in patients with osteoporosis than in patients with type 2 diabetes ( P<0.01) and in the control group ( P<0.001). Amylin plasma levels are decreased in patients with osteoporosis. Amylin deficiency in these patients may contribute to the development of osteoporosis. Amylin should be investigated in relation to the pharmacological treatment of osteoporosis.
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PMID:Amylin fasting plasma levels are decreased in patients with osteoporosis. 1460 1

Medical literature that has coalesced during the past two to three decades has identified adequate intake of nutrients from dairy foods as a common factor in the reduction of the disease burden of several common medical conditions. These include obesity, hypertension, type 2 diabetes, osteoporosis, kidney stones, certain outcomes of pregnancy, and some cancers. Treatment of these disorders, particularly cardiovascular, consumes a significant portion of the United States' healthcare budget. Drawing on accumulated data from prospective longitudinal studies and randomized controlled trials, this article summarizes the evidence of the net benefits of increased dairy food intake on these conditions, their outcomes, and their costs. Estimated improvements in outcomes were combined with available data on annual costs of the respective disorders. From the calculated annual impact, we generated first-year and fifth-year healthcare cost savings that would accrue if adult Americans simply increased their intake of dairy foods to the currently recommended 3 to 4 servings/d. Using conservative estimates of potential benefit, we project first-year savings of approximately 26 billion dollars and 5-year cumulative savings in excess of 200 billion dollars.
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PMID:Estimated healthcare savings associated with adequate dairy food intake. 1470 May 20

In 1989, reports suggested that the fetal environment, as reflected in birth size, was related to the risk of noncommunicable diseases in adult life. This association was first described for coronary heart disease but rapidly extended to include type 2 diabetes, osteoporosis, and metabolic and endocrine homeostasis. This led to the development of the fetal origins of adult disease paradigm, which resulted in a refocusing of research effort over the next 10 y to consider the lifelong consequences of perinatal influences on chronic diseases. Previously, perinatal influences had largely been seen in terms of teratogenic effects or acute birth injury rather than whether trajectories and responses made during early development had lifelong consequences. Indeed, in developmental biology, it is widely recognized that adaptive plastic responses during early development often have consequences for function in later adulthood. Although the relative importance of this newly recognized set of phenomena to the burden of human disease has been controversial, the research precipitated by those early observations has confirmed their robustness and started to provide a mechanistic basis to this biology. Two world congresses have been held to review progress in this research. Both have been characterized by a unique multidisciplinary attendance ranging from molecular, experimental, and developmental biologists to epidemiologists and health economists.
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PMID:Report on the 2nd World Congress on Fetal Origins of Adult Disease, Brighton, U.K., June 7-10, 2003. 1476 17

Several polymorphisms have been identified in the RAGE-promoter region that might modulate the outcome of disease. Here we analyse the association of a 63bp deletion (delta63) spanning from bp - 407 to bp - 345 with diabetic nephropathy. The deletion was determined using the polymerase chain reaction (PCR) in a cross-sectional study with 1087 patients with type 1 diabetes (n = 559) and type 2 diabetes (n = 528). 475 patients with osteoporosis served as disease independent control. The prevalence of the heterozygous genotype did not significantly differ between the three groups (type 1: 2.15 %, type 2: 2.27 %, controls: 1.47 %), indicating that heterozygous delta63 is not related to the manifestation of diabetes. Homozygous carriers were not identified in this study. The heterozygous delta63 genotype, was associated with a reduced prevalence of diabetic nephropathy in patients with type 2 diabetes (OR = 0.06; 95 % CI: [0.05, 0.07]), but not in patients with type 1 (OR = 1.49; 95 % CI: [1.14, 1.94]). We conclude, that patients with type 2 diabetes and the 63bp deletion in the promoter of RAGE seem to be protected from diabetic nephropathy. The observed difference between type 1 and type 2 diabetes might point to diverse pathomechanisms of nephropathy in both types of diabetes.
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PMID:A 63bp deletion in the promoter of rage correlates with a decreased risk for nephropathy in patients with type 2 diabetes. 1505 33

It is the position of the American Dietetic Association that children ages 2 to 11 years should achieve optimal physical and cognitive development, attain a healthy weight, enjoy food, and reduce the risk of chronic disease through appropriate eating habits and participation in regular physical activity. The health status of American children has generally improved over the past three decades. However, the number of children who are overweight has more than doubled among 2- to 5-year-old children and more than tripled among 6- to 11-year-old children, which has major health consequences. This increase in childhood overweight has broadened the focus of dietary guidance to address children's over consumption of energy-dense, nutrient-poor foods and beverages and physical activity patterns. Health promotion will help reduce diet-related risks of chronic degenerative diseases, such as cardiovascular disease, type 2 diabetes, cancer, obesity, and osteoporosis. This position paper reviews what US children are eating and explores trends in food and nutrient intakes as well as the impact of school meals on children's diets. Dietary recommendations and guidelines and the benefits of physical activity are also discussed. The roles of parents and caregivers in influencing the development of healthy eating behaviors are highlighted. The American Dietetic Association works with other allied health and food industry professionals to translate dietary recommendations and guidelines into achievable, healthful messages. Specific recommendations to improve the nutritional well-being of children are provided for dietetics professionals, parents, and caregivers.
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PMID:Position of the American Dietetic Association: Dietary guidance for healthy children ages 2 to 11 years. 1505 55

Postmenopausal women in Western societies are conscious of breast cancer as a potential cause of death and ill health, which they wish to avoid with the advice of their doctors. Yet many factors that predispose women to the development of cancer will have been laid down before the menopause, in their genetic makeup or during their adolescent years. Even in middle age it is important to take account of the intrinsic level of risk, and to give women advice tailored to their own individual risk level. This results from their family history, previous diseases such as benign breast disease, and previous treatment for breast cancer or Hodgkin's disease. For those at the highest level of risk, strategies will include regular screening, prophylactic mastectomy, and the use of chemoprevention agents, such as tamoxifen. These women should avoid hormone replacement therapy (HRT) and control their menopausal symptoms and osteoporosis through the use of other agents now available - venlafaxine for menopausal symptoms and bisphosphonates for osteoporosis. Raloxifene is an agent under trial that may be valuable for breast cancer control as well as for osteoporosis. Women at standard population risk will require less robust preventive strategies, which will include screening and lifestyle modification. Their decisions regarding HRT should now be modified by recent evidence of associated risks. Recent studies show that tibolone causes less mammographic density and has a lower relative risk of breast cancer than combined estrogen/progestogen preparations. There is limited evidence that controlling obesity, participating in exercise and adopting a diet low in fats and high in fruit and vegetables will alter risk at this age. These precautions will, however, reduce the risk of other diseases common in this age group, such as hypertension, heart disease, stroke, and type 2 diabetes mellitus. Alcohol, even in small amounts, is a risk factor for breast cancer. Given the cardioprotective effect of moderate alcohol intake, advice on alcohol must reflect the individual relative risk of cardiovascular disease and breast cancer. Personal risk assessment is relevant for all women. Screening and a healthy lifestyle are worthwhile approaches for all, with the more aggressive approaches such as chemoprevention and prophylactic surgery reserved for those who have substantially elevated levels of risk. Once the menopause has passed, screening is probably the most effective evidence-based tool for breast cancer control by early diagnosis.
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PMID:Strategies for managing breast cancer risk after the menopause. 1533 Jun 77

Prader-Willi syndrome (PWS) is characterized by hypothalamic dysfunction resulting in obesity, hypotonia, hypogonadism, and behavioral abnormalities. Clinical features of PWS resemble those of GH deficiency (decreased total lean body mass, IGF-I levels, and poor linear growth). Marked reductions in muscle mass are associated with diminished strength, physical function, and energy expenditure. Lifelong morbidities of PWS include osteoporosis, type 2 diabetes mellitus, respiratory disorders, and cardiorespiratory failure related to obesity and hypotonia. Recent studies show that GH therapy improves linear growth, final height, physical strength, and agility in patients with PWS. Some effects of GH therapy wane with time, however, and strategies for treating adults with PWS remain uncertain. In addition, deaths in markedly obese, GH-treated children with PWS have been reported, and a possible contribution of GH to these events has not yet been definitively excluded. Consequently, critical evaluation should continue of the long-term benefits, risks, and costs of GH therapy for patients with PWS.
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PMID:Growth hormone therapy for Prader-Willi syndrome: a critical appraisal. 1550 76

Thiazolidinediones (TZDs) increase peripheral tissue insulin sensitivity in patients with type 2 diabetes mellitus by activating the nuclear receptor peroxisome proliferator-activated receptor gamma (PPARgamma). In bone marrow stromal cell cultures and in vivo, activation of PPARgamma by high doses (20 mg/kg/day) of TZDs has been reported to alter stem cell differentiation by promoting commitment of progenitor cells to the adipocytic lineage while inhibiting osteoblastogenesis. Here, we have examined the in vivo effects of low-dose rosiglitazone (3 mg/kg/day) on bone, administered to mice by gavage for 90 days. Rosiglitazone-treated mice had increased weight when compared with controls, with no significant alterations in serum levels of glucose, calcium or parathyroid hormone (PTH). Bone mineral density (BMD) at the lumbar vertebrae (L1-L4), ilium/sacrum, and total body was diminished by rosiglitazone treatment. Histologically, bone was characterized by decreased trabecular bone volume and increased marrow space with no significant change in bone marrow adipocity. Decreased osteoblast number and activity due to increased apoptotic death of osteoblasts and osteocytes was apparent while osteoclast parameters and serum levels of osteocalcin, alkaline phosphatase activity, and leptin were unaltered by rosiglitazone treatment. Therefore, the imbalance in bone remodeling that follows rosiglitazone administration arises from increased apoptotic death of osteogenic cells and diminished bone formation leading to the observed decrease in trabecular bone volume and BMD. These novel in vivo effects of TZDs on bone are of clinical relevance as patients with type 2 diabetes mellitus and other insulin resistant states treated with these agents may potentially be at increased risk of osteoporosis.
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PMID:Rosiglitazone impacts negatively on bone by promoting osteoblast/osteocyte apoptosis. 1552 88

Since Albright first proposed the concept of "diabetic osteopenia", many studies have investigated the levels of bone mineral density (BMD) and the risk of osteoporosis in type 1 and type 2 diabetes. The presence of osteoporosis in type 1 diabetes seems to be a reliable evidence. On the other hand, there is still some controversy about the risk of osteoporosis in type 2 diabetes probably due to different pathogenesis, clinical stage and environmental factors. Although details of the pathogenic mechanisms are not fully understood, low insulin secretion, insulin resistance, hyperglycemia, adipocytokines and other diabetic complications including diabetic triopathy may determine changes in diabetic bone metabolism. Recent findings suggest that several drugs for life style-related disease such as statins, beta blockers and thiazolidinediones may have a potential role to promote bone formation other than their own therapeutic effects.
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PMID:[Diabetes and osteoporosis]. 1557 81


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