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Medical and Psychological Considerations for Carbohydrate-Restricted Diets in Youth With Type 1 Diabetes.
Gallagher KAS, DeSalvo D, Gregory J, Hilliard ME
(2019) Curr Diab Rep 19: 27
MeSH Terms: Adolescent, Blood Glucose, Child, Depression, Diabetes Mellitus, Type 1, Diet, Carbohydrate-Restricted, Feeding and Eating Disorders, Humans
Show Abstract · Added June 26, 2019
PURPOSE OF REVIEW - Given the challenges achieving recommended glycemic targets in youth with type 1 diabetes (T1D), providers may consider recommending carbohydrate-restricted diets (CRDs) to optimize glycemic control. The goal of the present review is to describe relevant literature on the potential medical and psychosocial benefits and risks of CRDs in youth with T1D.
RECENT FINDINGS - Limited data exist on the effects of CRDs in pediatric populations. Findings from studies with youth and adults are mixed; some indicate that CRDs may be associated with desirable medical outcomes, such as improved glycemic control and reduced HbA1c, which may contribute to positive psychological outcomes such as reduced diabetes distress and depressive symptoms. Others suggest that CRDs may also be associated with detrimental outcomes, including mineral deficiencies and suboptimal growth, and dietary restriction has been linked to greater diabetes distress, disordered eating, and diabetes management. More research is needed to evaluate benefits and risks of CRDs in youth. Providers should exercise caution when discussing CRDs with youth and families, particularly when considering CRDs for youth at elevated risk for eating disordered behavior.
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8 MeSH Terms
Human Semaphorin 3 Variants Link Melanocortin Circuit Development and Energy Balance.
van der Klaauw AA, Croizier S, Mendes de Oliveira E, Stadler LKJ, Park S, Kong Y, Banton MC, Tandon P, Hendricks AE, Keogh JM, Riley SE, Papadia S, Henning E, Bounds R, Bochukova EG, Mistry V, O'Rahilly S, Simerly RB, INTERVAL, UK10K Consortium, Minchin JEN, Barroso I, Jones EY, Bouret SG, Farooqi IS
(2019) Cell 176: 729-742.e18
MeSH Terms: Adolescent, Adult, Animals, Body Weight, Cell Line, Child, Child, Preschool, Disease Models, Animal, Eating, Energy Metabolism, Female, Genetic Variation, Homeostasis, Humans, Hypothalamus, Leptin, Male, Melanocortins, Mice, Mice, Inbred C57BL, Middle Aged, Nerve Tissue Proteins, Neurons, Obesity, Receptors, Cell Surface, Semaphorins, Young Adult, Zebrafish
Show Abstract · Added April 11, 2019
Hypothalamic melanocortin neurons play a pivotal role in weight regulation. Here, we examined the contribution of Semaphorin 3 (SEMA3) signaling to the development of these circuits. In genetic studies, we found 40 rare variants in SEMA3A-G and their receptors (PLXNA1-4; NRP1-2) in 573 severely obese individuals; variants disrupted secretion and/or signaling through multiple molecular mechanisms. Rare variants in this set of genes were significantly enriched in 982 severely obese cases compared to 4,449 controls. In a zebrafish mutagenesis screen, deletion of 7 genes in this pathway led to increased somatic growth and/or adiposity demonstrating that disruption of Semaphorin 3 signaling perturbs energy homeostasis. In mice, deletion of the Neuropilin-2 receptor in Pro-opiomelanocortin neurons disrupted their projections from the arcuate to the paraventricular nucleus, reduced energy expenditure, and caused weight gain. Cumulatively, these studies demonstrate that SEMA3-mediated signaling drives the development of hypothalamic melanocortin circuits involved in energy homeostasis.
Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.
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28 MeSH Terms
How and why do gastrointestinal peptides influence food intake?
Woods SC, May-Zhang AA, Begg DP
(2018) Physiol Behav 193: 218-222
MeSH Terms: Animals, Eating, Gastrointestinal Hormones, Humans, Peptides, Satiation
Show Abstract · Added July 2, 2018
Despite the ability of some gastrointestinal hormones to reliably reduce meal size when administered prior to a meal, it is not understood why the repeated administration or genetic knockout of these hormones appear largely ineffective in reducing food intake and body weight. Here, we review evidence that the ability of GI peptides such as cholecystokinin (CCK) to elicit satiation is a consequence of prior learning. Evidence includes first, that the ability of some of these signals to modify food intake depends upon past experience and is malleable with new experience. Additionally, the ability of CCK and other gut signals to reduce food intake may not be hard-wired; i.e., any so-called "satiation" signal that reduces food intake in a single-meal situation may not continue to do so over repeated trials. The individual will respond to the signal only so long as it provides reliable information about caloric content. If a particular signal becomes unreliable, the individual will rely on other signals to end meals. Thus, gut peptides/hormones have important metabolic effects such as mediating absorption, digestion, and many aspects of the distribution of ingested nutrients throughout the body; and, if they have been reliably associated with natural stimuli that mediate satiation, they also inform behavior.
Copyright © 2018. Published by Elsevier Inc.
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6 MeSH Terms
The glucagon-like peptide-1 receptor in the ventromedial hypothalamus reduces short-term food intake in male mice by regulating nutrient sensor activity.
Burmeister MA, Brown JD, Ayala JE, Stoffers DA, Sandoval DA, Seeley RJ, Ayala JE
(2017) Am J Physiol Endocrinol Metab 313: E651-E662
MeSH Terms: Acetyl-CoA Carboxylase, Adenylate Kinase, Animals, Body Composition, CHO Cells, Cricetulus, Dose-Response Relationship, Drug, Eating, Exenatide, Food, Glucagon-Like Peptide-1 Receptor, Glycolysis, Homeostasis, Male, Mice, Mice, Inbred C57BL, Peptides, Sensation, TOR Serine-Threonine Kinases, Venoms, Ventromedial Hypothalamic Nucleus
Show Abstract · Added October 23, 2017
Pharmacological activation of the glucagon-like peptide-1 receptor (GLP-1R) in the ventromedial hypothalamus (VMH) reduces food intake. Here, we assessed whether suppression of food intake by GLP-1R agonists (GLP-1RA) in this region is dependent on AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR). We found that pharmacological inhibition of glycolysis, and thus activation of AMPK, in the VMH attenuates the anorectic effect of the GLP-1R agonist exendin-4 (Ex4), indicating that glucose metabolism and inhibition of AMPK are both required for this effect. Furthermore, we found that Ex4-mediated anorexia in the VMH involved mTOR but not acetyl-CoA carboxylase, two downstream targets of AMPK. We support this by showing that Ex4 activates mTOR signaling in the VMH and Chinese hamster ovary (CHO)-K1 cells. In contrast to the clear acute pharmacological impact of the these receptors on food intake, knockdown of the VMH conferred no changes in energy balance in either chow- or high-fat-diet-fed mice, and the acute anorectic and glucose tolerance effects of peripherally dosed GLP-1RA were preserved. These results show that the VMH GLP-1R regulates food intake by engaging key nutrient sensors but is dispensable for the effects of GLP-1RA on nutrient homeostasis.
Copyright © 2017 the American Physiological Society.
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21 MeSH Terms
Oleoylethanolamide: A fat ally in the fight against obesity.
Brown JD, Karimian Azari E, Ayala JE
(2017) Physiol Behav 176: 50-58
MeSH Terms: Animals, Anti-Obesity Agents, Eating, Endocannabinoids, Humans, Intestinal Mucosa, Intestines, Obesity, Oleic Acids, Reward
Show Abstract · Added October 23, 2017
Obesity is a pandemic, gateway disease that has thrived in modern, sedentary, high calorie-eating societies. Left unchecked, obesity and obesity-related diseases will continue to plague future generations with heavy burdens on economies, healthcare systems, and the quality of life of billions. There is a significant need to elucidate basic physiological mechanisms and therapies that address this global health care crisis. Oleoylethanolamide (OEA) is an endocannabinoid-like lipid that induces hypophagia and reduces fat mass in rodents. For over a decade, PPAR-α has been the most widely accepted mediator of the hypophagic action of OEA via signaling to homeostatic brain centers. Recent evidence suggests that OEA may also reduce food intake via effects on dopamine and endocannabinoid signaling within hedonic brain centers. Limited study of OEA supplementation in humans has provided some encouraging insight into OEA-based weight loss therapy, but more thorough, controlled investigations are needed. As a potential link between homeostatic and hedonic regulation of food intake, OEA is a prime starting point for the development of more effective obesity therapies.
Copyright © 2017 Elsevier Inc. All rights reserved.
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10 MeSH Terms
The Hypothalamic Glucagon-Like Peptide 1 Receptor Is Sufficient but Not Necessary for the Regulation of Energy Balance and Glucose Homeostasis in Mice.
Burmeister MA, Ayala JE, Smouse H, Landivar-Rocha A, Brown JD, Drucker DJ, Stoffers DA, Sandoval DA, Seeley RJ, Ayala JE
(2017) Diabetes 66: 372-384
MeSH Terms: Animals, Body Composition, Diet, High-Fat, Eating, Energy Metabolism, Exenatide, Gene Knockdown Techniques, Glucagon-Like Peptide 1, Glucagon-Like Peptide-1 Receptor, Glucose, Glucose Tolerance Test, Homeostasis, Hypothalamus, Incretins, Liraglutide, Male, Mice, Neurons, Paraventricular Hypothalamic Nucleus, Peptides, Pro-Opiomelanocortin, Venoms, Weight Gain
Show Abstract · Added October 23, 2017
Pharmacological activation of the hypothalamic glucagon-like peptide 1 (GLP-1) receptor (GLP-1R) promotes weight loss and improves glucose tolerance. This demonstrates that the hypothalamic GLP-1R is sufficient but does not show whether it is necessary for the effects of exogenous GLP-1R agonists (GLP-1RA) or endogenous GLP-1 on these parameters. To address this, we crossed mice harboring floxed Glp1r alleles to mice expressing Nkx2.1-Cre to knock down Glp1r expression throughout the hypothalamus (GLP-1RKD). We also generated mice lacking Glp1r expression specifically in two GLP-1RA-responsive hypothalamic feeding nuclei/cell types, the paraventricular nucleus (GLP-1RKD) and proopiomelanocortin neurons (GLP-1RKD). Chow-fed GLP-1RKD mice exhibited increased food intake and energy expenditure with no net effect on body weight. When fed a high-fat diet, these mice exhibited normal food intake but elevated energy expenditure, yielding reduced weight gain. None of these phenotypes were observed in GLP-1RKD and GLP-1RKD mice. The acute anorectic and glucose tolerance effects of peripherally dosed GLP-1RA exendin-4 and liraglutide were preserved in all mouse lines. Chronic liraglutide treatment reduced body weight in chow-fed GLP-1RKD mice, but this effect was attenuated with high-fat diet feeding. In sum, classic homeostatic control regions are sufficient but not individually necessary for the effects of GLP-1RA on nutrient homeostasis.
© 2017 by the American Diabetes Association.
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23 MeSH Terms
Disgust proneness and associated neural substrates in obesity.
Watkins TJ, Di Iorio CR, Olatunji BO, Benningfield MM, Blackford JU, Dietrich MS, Bhatia M, Theiss JD, Salomon RM, Niswender K, Cowan RL
(2016) Soc Cogn Affect Neurosci 11: 458-65
MeSH Terms: Adult, Body Mass Index, Brain Mapping, Cerebral Cortex, Eating, Emotions, Female, Food, Food Contamination, Functional Laterality, Humans, Hunger, Hyperphagia, Magnetic Resonance Imaging, Male, Neuropsychological Tests, Obesity, Photic Stimulation
Show Abstract · Added February 15, 2016
Defects in experiencing disgust may contribute to obesity by allowing for the overconsumption of food. However, the relationship of disgust proneness and its associated neural locus has yet to be explored in the context of obesity. Thirty-three participants (17 obese, 16 lean) completed the Disgust Propensity and Sensitivity Scale-Revised and a functional magnetic resonance imaging paradigm where images from 4 categories (food, contaminates, contaminated food or fixation) were randomly presented. Independent two-sample t-tests revealed significantly lower levels of Disgust Sensitivity for the obese group (mean score = 14.7) compared with the lean group (mean score = 17.6, P = 0.026). The obese group had less activation in the right insula than the lean group when viewing contaminated food images. Multiple regression with interaction analysis revealed one left insula region where the association of Disgust Sensitivity scores with activation differed by group when viewing contaminated food images. These interaction effects were driven by the negative correlation of Disgust Sensitivity scores with beta values extracted from the left insula in the obese group (r = -0.59) compared with a positive correlation in the lean group (r = 0.65). Given these body mass index-dependent differences in Disgust Sensitivity and neural responsiveness to disgusting food images, it is likely that altered Disgust Sensitivity may contribute to obesity.
© The Author (2015). Published by Oxford University Press. For Permissions, please email: journals.permissions@oup.com.
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18 MeSH Terms
Retention of sedentary obese visceral white adipose tissue phenotype with intermittent physical activity despite reduced adiposity.
Wainright KS, Fleming NJ, Rowles JL, Welly RJ, Zidon TM, Park YM, Gaines TL, Scroggins RJ, Anderson-Baucum EK, Hasty AH, Vieira-Potter VJ, Padilla J
(2015) Am J Physiol Regul Integr Comp Physiol 309: R594-602
MeSH Terms: Adipokines, Adiposity, Age Factors, Animals, Disease Models, Animal, Eating, Endoplasmic Reticulum Stress, Gene Expression Regulation, Inflammation Mediators, Intra-Abdominal Fat, Male, Mice, Inbred C57BL, Motor Activity, Obesity, Oxidative Stress, Phenotype, Running, Sedentary Behavior
Show Abstract · Added September 28, 2015
Regular physical activity is effective in reducing visceral white adipose tissue (AT) inflammation and oxidative stress, and these changes are commonly associated with reduced adiposity. However, the impact of multiple periods of physical activity, intercalated by periods of inactivity, i.e., intermittent physical activity, on markers of AT inflammation and oxidative stress is unknown. In the present study, 5-wk-old male C57BL/6 mice were randomized into three groups (n = 10/group): sedentary, regular physical activity, and intermittent physical activity, for 24 wk. All animals were singly housed and fed a diet containing 45% kcal from fat. Regularly active mice had access to voluntary running wheels throughout the study period, whereas intermittently active mice had access to running wheels for 3-wk intervals (i.e., 3 wk on/3 wk off) throughout the study. At death, regular and intermittent physical activity was associated with similar reductions in visceral AT mass (approximately -24%, P < 0.05) relative to sedentary. However, regularly, but not intermittently, active mice exhibited decreased expression of visceral AT genes related to inflammation (e.g., monocyte chemoattractant protein 1), immune cell infiltration (e.g., CD68, CD11c, F4/80, CD11b/CD18), oxidative stress (e.g., p47 phagocyte oxidase), and endoplasmic reticulum stress (e.g., CCAAT enhancer-binding protein homologous protein; all P < 0.05). Furthermore, regular, but not intermittent, physical activity was associated with a trend toward improvement in glucose tolerance (P = 0.059). Collectively, these findings suggest that intermittent physical activity over a prolonged period of time may lead to a reduction in adiposity but with retention of a sedentary obese white AT and metabolic phenotype.
Copyright © 2015 the American Physiological Society.
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18 MeSH Terms
Noninvasive biomagnetic detection of intestinal slow wave dysrhythmias in chronic mesenteric ischemia.
Somarajan S, Muszynski ND, Cheng LK, Bradshaw LA, Naslund TC, Richards WO
(2015) Am J Physiol Gastrointest Liver Physiol 309: G52-8
MeSH Terms: Chronic Disease, Eating, Electrodiagnosis, Electromyography, Gastrointestinal Motility, Humans, Jejunum, Magnetometry, Mesenteric Ischemia, Postprandial Period, Predictive Value of Tests, Time Factors
Show Abstract · Added April 26, 2016
Chronic mesenteric ischemia (CMI) is a challenging clinical problem that is difficult to diagnose noninvasively. Diagnosis early in the disease process would enable life-saving early surgical intervention. Previous studies established that superconducting quantum interference device (SQUID) magnetometers detect the slow wave changes in the magnetoenterogram (MENG) noninvasively following induction of mesenteric ischemia in animal models. The purpose of this study was to assess functional physiological changes in the intestinal slow wave MENG of patients with chronic mesenteric ischemia. Pre- and postoperative studies were conducted on CMI patients using MENG and intraoperative recordings using invasive serosal electromyograms (EMG). Our preoperative MENG recordings showed that patients with CMI exhibited a significant decrease in intestinal slow wave frequency from 8.9 ± 0.3 cpm preprandial to 7.4 ± 0.1 cpm postprandial (P < 0.01) that was not observed in postoperative recordings (9.3 ± 0.2 cpm preprandial and 9.4 ± 0.4 cpm postprandial, P = 0.86). Intraoperative recording detected multiple frequencies from the ischemic portion of jejunum before revascularization, whereas normal serosal intestinal slow wave frequencies were observed after revascularization. The preoperative MENG data also showed signals with multiple frequencies suggestive of uncoupling and intestinal ischemia similar to intraoperative serosal EMG. Our results showed that multichannel MENG can identify intestinal slow wave dysrhythmias in CMI patients.
Copyright © 2015 the American Physiological Society.
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12 MeSH Terms
Chronic overeating impairs hepatic glucose uptake and disposition.
Coate KC, Kraft G, Shiota M, Smith MS, Farmer B, Neal DW, Williams P, Cherrington AD, Moore MC
(2015) Am J Physiol Endocrinol Metab 308: E860-7
MeSH Terms: Animals, Blood Glucose, C-Peptide, Chronic Disease, Dogs, Eating, Glucose, Glucose Clamp Technique, Hyperphagia, Insulin, Liver, Male, Weight Gain
Show Abstract · Added July 24, 2015
Dogs consuming a hypercaloric high-fat and -fructose diet (52 and 17% of total energy, respectively) or a diet high in either fructose or fat for 4 wk exhibited blunted net hepatic glucose uptake (NHGU) and glycogen deposition in response to hyperinsulinemia, hyperglycemia, and portal glucose delivery. The effect of a hypercaloric diet containing neither fructose nor excessive fat has not been examined. Dogs with an initial weight of ≈25 kg consumed a chow and meat diet (31% protein, 44% carbohydrate, and 26% fat) in weight-maintaining (CTR; n = 6) or excessive (Hkcal; n = 7) amounts for 4 wk (cumulative weight gain 0.0 ± 0.3 and 1.5 ± 0.5 kg, respectively, P < 0.05). They then underwent clamp studies with infusions of somatostatin and intraportal insulin (4× basal) and glucagon (basal). The hepatic glucose load was doubled with peripheral (Pe) glucose infusion for 90 min (P1) and intraportal glucose at 4 mg·kg(-1)·min(-1) plus Pe glucose for the final 90 min (P2). NHGU was blunted (P < 0.05) in Hkcal during both periods (mg·kg(-1)·min(-1); P1: 1.7 ± 0.2 vs. 0.3 ± 0.4; P2: 3.6 ± 0.3 vs. 2.3 ± 0.4, CTR vs. Hkcal, respectively). Terminal hepatic glucokinase catalytic activity was reduced nearly 50% in Hkcal vs. CTR (P < 0.05), although glucokinase protein did not differ between groups. In Hkcal vs. CTR, liver glycogen was reduced 27% (P < 0.05), with a 91% increase in glycogen phosphorylase activity (P < 0.05) but no significant difference in glycogen synthase activity. Thus, Hkcal impaired NHGU and glycogen synthesis compared with CTR, indicating that excessive energy intake, even if the diet is balanced and nutritious, negatively impacts hepatic glucose metabolism.
Copyright © 2015 the American Physiological Society.
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13 MeSH Terms