Role of opiate peptides in regulating energy balance

2009 ◽  
pp. 232-265 ◽  
Author(s):  
Richard J. Bodnar ◽  
Allen S. Levine
Keyword(s):  
Energy Balance ◽  
Opiate Peptides

Influence of Magnetic Fields on Solar Hydrodynamics: Experimental Results

1977 ◽  
Vol 36 ◽  
pp. 143-180 ◽  
Author(s):  
J.O. Stenflo
Keyword(s):  
Solar Activity ◽  
Energy Balance ◽  
Magnetic Fields ◽  
Solar Atmosphere ◽  
General Problem ◽  
Solar Rotation ◽  
Active Regions ◽  
Physical Conditions ◽  
Dynamic Phenomena

It is well-known that solar activity is basically caused by the Interaction of magnetic fields with convection and solar rotation, resulting in a great variety of dynamic phenomena, like flares, surges, sunspots, prominences, etc. Many conferences have been devoted to solar activity, including the role of magnetic fields. Similar attention has not been paid to the role of magnetic fields for the overall dynamics and energy balance of the solar atmosphere, related to the general problem of chromospheric and coronal heating. To penetrate this problem we have to focus our attention more on the physical conditions in the ‘quiet’ regions than on the conspicuous phenomena in active regions.

Ghrelin and Obesity-An Update

2017 ◽  
Vol 9 (1) ◽  
Author(s):  
Gandhi M. ◽  
Swaminathan S.
Keyword(s):  
Diabetes Mellitus ◽  
Cardiac Output ◽  
Energy Balance ◽  
Vascular Resistance ◽  
The Body ◽  
Ghrelin Receptor ◽  
Type2 Diabetes ◽  
Type2 Diabetes Mellitus ◽  
Natural Hormones

Ghrelin as human natural hormones is involved in fundamental regulatory process of eating and energy balance. It is a stomach derived hormone that acts as at the ghrelin receptor in multiple tissues throughout to the body. Its properties includes increasing appetite, decreasing systemic inflammation, decreasing vascular resistance ,increasing cardiac output, increasing glucose and IGF-1 levels, Hence it may play a significant role in Diabetes mellitus. Many studies have linked ghrelin to obesity and this paper is an attempt to bring out recent findings on the role of ghrelin in Diabetes Mellitus, particularly type2 Diabetes mellitus.

Role of ghrelin in the regulation of energy balance in adult male albino rats

2020 ◽  
Vol 33 (1) ◽  
pp. 30-38
Author(s):  
Naglaa Y. Nafeh ◽  
Mona A. Said
Keyword(s):  
Energy Balance ◽  
Adult Male ◽  
Albino Rats

scholarly journals Ubc9 deletion in adipocytes causes lipoatrophy in mice

2020 ◽  
Author(s):  
Aaron R. Cox ◽  
Natasha Chernis ◽  
Kang Ho Kim ◽  
Peter M. Masschelin ◽  
Pradip K. Saha ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Balance ◽  
Hepatic Steatosis ◽  
Postnatal Growth ◽  
Endocrine Control ◽  
Brown Adipocytes ◽  
Human Adipocyte ◽  
White Adipocyte ◽  
Adipose Tissue Depots

ABSTRACTObjectiveWhite adipose tissue (WAT) expansion regulates energy balance and overall metabolic homeostasis. WAT absence or loss occurring through lipodystrophy and lipoatrophy contributes to the development of dyslipidemia, hepatic steatosis, and insulin resistance. We previously demonstrated the sole small ubiquitin-like modifier (SUMO) E2-conjuguating enzyme Ubc9 represses human adipocyte differentiation. Germline and other tissue-specific deletions of Ubc9 frequently cause lethality in mice. As a result, the role of Ubc9 during WAT development remains unknown.MethodsTo determine how Ubc9 impacts body composition and energy balance, we generated adipocyte-specific Ubc9 knockout mice (Ubc9a-KO). CRISPR/Cas9 gene editing inserted loxP sites flanking exons 3 and 4 at the Ubc9 locus. Subsequent genetic crosses to AdipoQ-Cre transgenic mice allowed deletion of Ubc9 in white and brown adipocytes. We measured multiple metabolic endpoints that describe energy balance and carbohydrate metabolism in Ubc9a-KO and littermate controls during postnatal growth.ResultsTo our surprise, Ubc9a-KO mice developed hyperinsulinemia and hepatic steatosis. Global energy balance defects emerged from dysfunctional WAT marked by pronounced local inflammation, loss of serum adipokines, hepatomegaly, and near absence of major adipose tissue depots. We observed progressive lipoatrophy that commences in the early adolescent period.ConclusionsOur results demonstrate that Ubc9 expression in mature adipocytes is essential for maintaining WAT expansion. Deletion of Ubc9 in fat cells compromised and diminished adipocyte function that provoked WAT inflammation and ectopic lipid accumulation in the liver. Our findings reveal an indispensable role for Ubc9 during white adipocyte expansion and endocrine control of energy balance.

scholarly journals Olfactory Dysfunction: A Complication of Diabetes or a Factor That Complicates Glucose Metabolism? A Narrative Review

2021 ◽  
Vol 10 (23) ◽  
pp. 5637
Author(s):  
Evanthia Gouveri ◽  
Nikolaos Papanas
Keyword(s):  
Diabetes Mellitus ◽  
Peripheral Neuropathy ◽  
Energy Balance ◽  
Glucose Metabolism ◽  
Microvascular Complications ◽  
Diabetic Complication ◽  
Olfactory Dysfunction ◽  
Narrative Review ◽  
Central Neuropathy

The present narrative review presents emerging data regarding the association between diabetes mellitus and olfactory dysfunction and discusses the role of olfactory dysfunction in glucose metabolism. We searched relevant published articles in PubMed and Google Scholar until October 2021. Main key words included “olfactory dysfunction”, “diabetes mellitus”, and “glucose metabolism”. Olfactory dysfunction has been associated with diabetes mellitus. Furthermore, it has been proposed to be a diabetic complication, given that it has been linked with microvascular complications, such as diabetic peripheral neuropathy. Interestingly, it has been suggested that olfactory dysfunction is a manifestation of central neuropathy in diabetes, a hypothesis based on the observation that diabetes, olfactory dysfunction, and cognitive decline often coexist. However, evidence is limited and inconsistent. More importantly, olfactory and endocrine systems are closely linked, and olfactory dysfunction plays a significant role in glucose metabolism and obesity. Indeed, food behaviour and energy balance are influenced by olfaction status.

scholarly journals Reduced Liver-Specific PGC1a Increases Susceptibility for Short-Term Diet-induced Weight Gain in Male Mice

2020 ◽  
Author(s):  
E. Matthew Morris ◽  
Roberto D. Noland ◽  
Michael E. Ponte ◽  
Michelle L. Montonye ◽  
Julie A. Christianson ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Weight Gain ◽  
Energy Metabolism ◽  
Energy Balance ◽  
Fatty Acid Oxidation ◽  
Positive Energy ◽  
Acid Oxidation ◽  
Male Mice ◽  
Short Term

AbstractCentral integration of peripheral neural signals is one mechanism by which systemic energy homeostasis is regulated. Previous work described increased acute food intake following chemical reduction of hepatic fatty acid oxidation and ATP levels, which was prevented by common hepatic branch vagotomy (HBV). However, possible offsite actions of the chemical compounds confound the precise role of liver energy metabolism. Herein, we used a liver-specific PGC1a heterozygous (LPGC1a) mouse model, with associated reductions in mitochondrial fatty acid oxidation and respiratory capacity, to assess the role of liver energy metabolism in systemic energy homeostasis. LPGC1a male mice have 70% greater high-fat/high-sucrose (HFHS) diet-induced weight gain and 35% greater positive energy balance compared to wildtype (WT) (p<0.05). The greater energy balance was associated with altered feeding behavior and lower activity energy expenditure during HFHS in LPGC1a males. Importantly, no differences in HFHS-induced weight gain or energy metabolism was observed between female WT and LPGC1a mice. WT and LPGC1a mice underwent sham or HBV to assess whether vagal signaling was involved in HFHS-induced weight gain of male LPGC1a mice. HBV increased HFHS-induced weight gain (85%, p<0.05) in male WT, but not LPGC1a mice. As above, sham LPGC1a males gain 70% more weight during short-term HFHS feeding than sham WT (p<0.05). These data demonstrate a sexspecific role of reduced liver energy metabolism in acute diet-induced weight gain, and the need of more nuanced assessment of the role of vagal signaling in short-term diet-induced weight gain.Key Points SummaryReduced liver PGC1a expression results in reduced mitochondrial fatty acid oxidation and respiratory capacity in male mice.Male mice with reduced liver PGC1a expression (LPGC1a) demonstrate greater short-term high-fat/high-sucrose diet-induced weight gain compared to wildtype.Greater positive energy balance during HFHS feeding in male LPGC1a mice is associated with altered food intake patterns and reduced activity energy expenditure.Female LPGC1a mice do not have differences in short-term HFHS-induced body weight gain or energy metabolism compared to wildtype.Disruption of vagal signaling through common hepatic branch vagotomy increases short-term HFHS-induced weight gain in male wildtype mice, but does not alter male LPGC1a weight gain.

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