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1 nism maintaining whole-body metabolism under overnutrition.
2 cing the simultaneous presence of under- and overnutrition.
3 a leptinergic blockade in adipocytes during overnutrition.
4 asis in nonadipose tissues during periods of overnutrition.
5 meostatic capacity to compensate for chronic overnutrition.
6 odulating the beta-cell cellular response to overnutrition.
7 matory responses in the liver in response to overnutrition.
8 tential lipotoxins, in a Drosophila model of overnutrition.
9 storage pathways during periods of maternal overnutrition.
10 may be lipotoxins that reduce fitness during overnutrition.
11 besity prevents thermogenic compensation for overnutrition.
12 ractions in offspring responding to maternal overnutrition.
13 n during development on exposure to maternal overnutrition.
14 s linked to caloric imbalance as a result of overnutrition.
15 posure to excessive daily caloric intake and overnutrition.
16 increased beta-cell number in the absence of overnutrition.
17 rvation and exerting a paradoxical effect in overnutrition.
18 rities, and a focus on undernutrition versus overnutrition.
19 ed insulin secretion in response to maternal overnutrition.
20 gy under conditions of normality and chronic overnutrition.
21 rtification, possibly resulting in under- or overnutrition.
22 he hypothesis that AMPK is protective during overnutrition.
23 cts (AGEs), which enhance appetite and cause overnutrition.
25 es and biomarkers related to both under- and overnutrition across 21 islands, including obesity, anem
26 ntestinally derived GIP, as a consequence of overnutrition, acts in the brain to impair hypothalamic
29 calorically rich diets combined with chronic overnutrition and a sedentary lifestyle in Western socie
30 ly accepted that those conditions arise from overnutrition and a sedentary lifestyle, which lead to i
31 ator of macrophage activation in response to overnutrition and a therapeutic target for ameliorating
34 s may represent an intermediate link between overnutrition and certain pathological mechanisms underl
37 e pathophysiology in diseases that integrate overnutrition and inflammation, such as nonalcoholic ste
38 as metainflammation, develops in response to overnutrition and is a major player in the regulation of
39 a global epidemic and are driven by chronic overnutrition and multiple genetic susceptibility factor
40 king early promoters of diabetes, especially overnutrition and obesity, to vascular insulin resistanc
41 nd inflammation, and the indirect effects of overnutrition and obesity-risk factors for colorectal ca
42 ssential for healthy adaptation of the AT to overnutrition and prevents aberrant propagation of negat
43 metabolic inflexibility that underlies both overnutrition and protein malnutrition-associated fatty
46 SirT1 to levels similar to those seen during overnutrition and studied SirT1-overexpressing transgeni
50 double burden of malnutrition (DBM), whereby overnutrition and undernutrition coexist within the same
51 o investigate the effects of early postnatal overnutrition and undernutrition on the maturation of hy
53 kinase e and TBK1, which are upregulated by overnutrition, and may therefore be suitable potential t
54 upregulated in the liver under conditions of overnutrition, and mice globally lacking the gene (CREBH
57 owever, in wealthy countries, the effects of overnutrition are prominent, where high supplies particu
58 al regulatory systems and therefore promotes overnutrition-associated diseases remains unexplored.
60 malnourishment and diseases associated with overnutrition, both research and technological breakthro
61 ng-chain fatty acids (FAs) during periods of overnutrition by increasing the beta-oxidative metabolis
65 ough leptin deficiency or leptin resistance, overnutrition causes disease of nonadipose tissues with
67 ernutrition, micronutrient deficiencies, and overnutrition-continues to rise globally, driven by comp
74 ive interventions on both undernutrition and overnutrition, employing robust study designs (individua
76 hese pathways are thought to be activated by overnutrition, especially increased intake of milk, dair
77 overaccumulate in nonadipose tissues during overnutrition, fatty acids enter deleterious pathways su
78 orms nutrient signals into oncogenic signals.Overnutrition has been linked to increased risk of cance
79 uld be given to the specificity of the fetal overnutrition hypothesis in terms of which aspects of th
80 The findings were consistent with the fetal overnutrition hypothesis only in relation to birth weigh
88 th acceleration as a consequence of relative overnutrition in infancy has been suggested to increase
91 n in the pars intercerebralis mimics chronic overnutrition in that it causes metabolic learning impai
94 egulation of Pparg expression in response to overnutrition in utero might underpin programmed cardiac
95 dings support an adverse effect of relative "overnutrition" in infancy on long-term cardiovascular di
96 lth complications associated with under- and overnutrition, including musculoskeletal impairment, imm
98 promoter methylation in response to chronic overnutrition increases the number of TH+ beta-cells, co
101 ied Fgf1 signaling as a key component of the overnutrition-induced beta-cell differentiation signal i
107 em might be causative for the development of overnutrition-induced metabolic syndrome and related dis
108 and resulting from insulin resistance and/or overnutrition induces a compensatory increase in beta-ce
109 rodent models has shown that early postnatal overnutrition induces excess adiposity and other compone
110 sed by nutrient deprivation and inhibited by overnutrition, inflammation, and hypersecretion of certa
113 ldhood malnutrition, both undernutrition and overnutrition, is a major health concern in many low- an
114 Malnutrition, which encompasses under- and overnutrition, is responsible for an enormous morbidity
115 ther, our data indicate that early postnatal overnutrition leads to a reduction in spontaneous physic
118 these innate immune cell-elicited signals in overnutrition may be modulated by weight loss, such as t
119 increased Plin5 expression that occurs with overnutrition may play an important role in preventing h
121 We conclude that in this model of maternal overnutrition, mitochondrial alterations occur before th
123 e the additive effects of excitotoxicity and overnutrition on beta-cell function and gene expression,
124 ical to examine the consequences of maternal overnutrition on the development of brain circuitry that
125 ccount the impact of both undernutrition and overnutrition on the microbiota and on infants' health o
126 Here, we showed that during either chronic overnutrition or acute induction of ER stress, Them2 and
128 any number of sources (e.g. viral infection, overnutrition, or oncologic burden) is a global health p
129 Consistent reporting of undernutrition and overnutrition outcomes in all nutrition interventions is
132 nes that regulate the adipogenic response to overnutrition profoundly influences the age of onset and
134 ndernutrition affect energy metabolism, with overnutrition raising energy expenditure and undernutrit
136 ted with adipose tissue dysfunction and many overnutrition-related metabolic diseases including type
137 accompanies fasting, insulin deficiency, and overnutrition, responses that are defective in obesity a
139 However, the molecular mechanisms underlying overnutrition stress in islet cells is not well understo
140 Several studies have reported that chronic overnutrition, such as excessive consumption of fats (hi
141 are common worldwide and include diseases of overnutrition, such as obesity, or undernutrition, such
142 evels in adults, and both undernutrition and overnutrition suppress gonadotropins: thus, the gonadotr
144 alnutrition, whether it be undernutrition or overnutrition, that is, in terms of both stunted and ove
147 a growing body of evidence linking maternal overnutrition to obesity and psychopathology that can be
148 tide (GIP)] and its receptor (GIPR) may link overnutrition to obesity, insulin resistance, and type 2
149 tic vascular disease, owing to the spread of overnutrition, underexertion, obesity, insulin resistanc
150 necessary to offset the metabolic burden of overnutrition was tested using chow-fed and high-fat (HF
151 or phosphatidylcholine (PC), particularly in overnutrition, where reduced phospholipid levels have be
152 cted animals from the deleterious effects of overnutrition, whereas downregulating PGRP-SC2 produced
153 In our study, we subjected human islets to overnutrition with 25 mmol/L glucose and 0.5 mmol/L palm
155 biogenesis and their key regulator Ppargc1a Overnutrition worsened excitotoxicity-induced mitochondr