ライフサイエンスコーパス: overnutrition

1 increased beta-cell number in the absence of overnutrition.

2 rvation and exerting a paradoxical effect in overnutrition.

3 rities, and a focus on undernutrition versus overnutrition.

4 s linked to caloric imbalance as a result of overnutrition.

5 ed insulin secretion in response to maternal overnutrition.

6 gy under conditions of normality and chronic overnutrition.

7 rtification, possibly resulting in under- or overnutrition.

8 cts (AGEs), which enhance appetite and cause overnutrition.

9 posure to excessive daily caloric intake and overnutrition.

10 cing the simultaneous presence of under- and overnutrition.

11 a leptinergic blockade in adipocytes during overnutrition.

12 asis in nonadipose tissues during periods of overnutrition.

13 The oncogenic mechanisms of overnutrition, a confirmed independent cancer risk facto

14 Prenatal overnutrition affects development into adulthood and inf

15 Nutritional transition (from under- to overnutrition) among women of reproductive age (15-49 y)

16 ly accepted that those conditions arise from overnutrition and a sedentary lifestyle, which lead to i

17 and thus posit that decreases in SirT1 link overnutrition and adipose tissue inflammation.

18 pothalamic microinflammation, in translating overnutrition and aging into complex outcomes.

19 s may represent an intermediate link between overnutrition and certain pathological mechanisms underl

20 ially relevant to accelerated brain aging by overnutrition and diabetes.

21 king early promoters of diabetes, especially overnutrition and obesity, to vascular insulin resistanc

22 nd inflammation, and the indirect effects of overnutrition and obesity-risk factors for colorectal ca

23 ong developed countries, and mainly reflects overnutrition and sedentary lifestyle.

24 SirT1 to levels similar to those seen during overnutrition and studied SirT1-overexpressing transgeni

25 lin resistance, and other deadly sequelae of overnutrition and underexertion.

26 Both overnutrition and undernutrition affect energy metabolis

27 Overnutrition and undernutrition are major concerns in t

28 o investigate the effects of early postnatal overnutrition and undernutrition on the maturation of hy

29 Undernutrition and overnutrition are epidemics of the impoverished and the

30 al regulatory systems and therefore promotes overnutrition-associated diseases remains unexplored.

31 Overnutrition atypically activates hypothalamic IKKbeta/

32 malnourishment and diseases associated with overnutrition, both research and technological breakthro

33 ng-chain fatty acids (FAs) during periods of overnutrition by increasing the beta-oxidative metabolis

34 It is possible that overnutrition can lead to hyperglycemia and an increased

35 Overnutrition can promote liver cancer in mice and human

36 ough leptin deficiency or leptin resistance, overnutrition causes disease of nonadipose tissues with

37 election of BCL-2 overexpressing cells under overnutrition conditions.

38 Obesity and overnutrition during pregnancy affect fetal programming

39 Limiting overnutrition during pregnancy, early childhood, and pub

40 hese pathways are thought to be activated by overnutrition, especially increased intake of milk, dair

41 overaccumulate in nonadipose tissues during overnutrition, fatty acids enter deleterious pathways su

42 orms nutrient signals into oncogenic signals.Overnutrition has been linked to increased risk of cance

43 uld be given to the specificity of the fetal overnutrition hypothesis in terms of which aspects of th

44 The findings were consistent with the fetal overnutrition hypothesis only in relation to birth weigh

45 The fetal overnutrition hypothesis proposes that greater maternal

46 According to the fetal overnutrition hypothesis, intrauterine influences of mat

47 According to the developmental overnutrition hypothesis, this could lead offspring to h

48 erational change in BMI and tested the fetal overnutrition hypothesis.

49 findings provide some support for the fetal overnutrition hypothesis.

50 th acceleration as a consequence of relative overnutrition in infancy has been suggested to increase

51 macrophage influx into adipose tissue during overnutrition in rodents and humans.

52 n in the pars intercerebralis mimics chronic overnutrition in that it causes metabolic learning impai

53 ns of social distribution of both under- and overnutrition in the Indian context.

54 dings support an adverse effect of relative "overnutrition" in infancy on long-term cardiovascular di

55 lth complications associated with under- and overnutrition, including musculoskeletal impairment, imm

56 In conclusion, overnutrition increases and adenovirus-induced hyperlept

57 Maternal overnutrition increases the risk of long-term metabolic

58 ied Fgf1 signaling as a key component of the overnutrition-induced beta-cell differentiation signal i

59 Fgf1 was confirmed as the overnutrition-induced beta-cell differentiation signal,

60 em might be causative for the development of overnutrition-induced metabolic syndrome and related dis

61 and resulting from insulin resistance and/or overnutrition induces a compensatory increase in beta-ce

62 rodent models has shown that early postnatal overnutrition induces excess adiposity and other compone

63 Overnutrition is associated with chronic inflammation in

64 Malnutrition, which encompasses under- and overnutrition, is responsible for an enormous morbidity

65 ther, our data indicate that early postnatal overnutrition leads to a reduction in spontaneous physic

66 In adipose tissue chronic overnutrition leads to macrophage infiltration, resultin

67 These data indicate that overnutrition leads to the development of a hypoxic stat

68 Chronic overnutrition (obesity) might thus be a proinflammatory

69 ical to examine the consequences of maternal overnutrition on the development of brain circuitry that

70 Here, we showed that during either chronic overnutrition or acute induction of ER stress, Them2 and

71 any number of sources (e.g. viral infection, overnutrition, or oncologic burden) is a global health p

72 It is now well known that chronic overnutrition produces a unique form of inflammation in

73 nes that regulate the adipogenic response to overnutrition profoundly influences the age of onset and

74 Uncompensated overnutrition promotes obesity, but the controls of chil

75 ndernutrition affect energy metabolism, with overnutrition raising energy expenditure and undernutrit

76 In zebrafish, overnutrition rapidly induces compensatory beta-cell dif

77 ted with adipose tissue dysfunction and many overnutrition-related metabolic diseases including type

78 accompanies fasting, insulin deficiency, and overnutrition, responses that are defective in obesity a

79 evels in adults, and both undernutrition and overnutrition suppress gonadotropins: thus, the gonadotr

80 ays, and it is compromised in the setting of overnutrition to cause insulin resistance.

81 tide (GIP)] and its receptor (GIPR) may link overnutrition to obesity, insulin resistance, and type 2

82 tic vascular disease, owing to the spread of overnutrition, underexertion, obesity, insulin resistanc

83 cted animals from the deleterious effects of overnutrition, whereas downregulating PGRP-SC2 produced