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)

In 1986, house mice in a small defined area of inner Birmingham were reported as not taking a variety of rodenticides from bait containers, a phenomenon labelled 'behavioural resistance'. This study investigated behavioural resistance by comparing the food preferences of West Midlands behaviourally resistant (WMBR) mice with those of normal (BC) mice. Nine bait boxes each containing one of nine different foods (cheese, chicken, tuna fish, peanut butter, canary seed, Cat stars, wheat, PCD (MOD) pellets and Non-tox) were introduced to 12 WMBR and seven BC sites (Experiment 1). The experiment was repeated in the laboratory with six pens of WMBR and six of BC mice (Experiment 2), and to investigate whether the preferences had a genetic basis the offspring were similarly assayed (Experiment 3). In each experiment the consumption of each food was measured over 7 days and the droppings around the bait boxes were counted to assess mouse activity. Food neophobia was noted in some populations of BC mice. Tested in the wild and in the laboratory WMBR mice showed an aversion to foods containing cereals, as did their offspring. These results, with other lines of evidence, strongly suggest that cereal aversion in WMBR mice has a physiological/genetic basis. Since cereal aversion allows WMBR mice to survive cereal-based rodenticidal baits, we conclude that WMBR mice have genetically based behaviours that allow them to survive poisoning regimes that kill other strains.
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PMID:Cereal aversion in behaviourally resistant house mice in Birmingham, UK. 1070 Jun 30

The purpose of this study was to assess the effects of a commercially available weight loss program on weight and glycemic control among obese patients with type 2 diabetes. Participants included 69 patients (49 females, 20 males) with type 2 diabetes who had a mean +/- SD age of 52.2 +/- 9.5 years, a body mass index of 39.0 +/- 6.2 kg/m(2), and hemoglobin A1c (HbA1c) of 7.5 +/- 1.6%. Over half (52.2%) of the participants were African American. Participants were randomly assigned to: 1) a portion-controlled diet (NutriSystem D) (PCD) or 2) a diabetes support and education (DSE) program. After the initial 3 months, the PCD group continued on the PCD for the remaining 3 months, and the DSE group crossed over to PCD for the remaining 3 months. The primary comparison for this study was at 3 months. At 3 months, the PCD group lost significantly more weight (7.1 +/- 4%) than the DSE group (0.4 +/- 2.3%) (P < 0.0001). From 3 to 6 months the change in weight for both groups was statistically significant. After 3 months, the PCD group had greater reductions in HbA1c than the DSE group (-0.88 +/- 1.1 vs 0.03 +/- 1.09; P < 0.001). From 3 to 6 months the PCD group had no further change in HbA1c, while the DSE group showed a significant reduction. These data suggest that obese patients with type 2 diabetes will experience significant improvements in weight, glycemic control, and cardiovascular disease risk factors after the use of a commercially available weight management program.
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PMID:The effects of a commercially available weight loss program among obese patients with type 2 diabetes: a randomized study. 1982 Feb 80