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No insulating effect of obesity
Stockholms universitet, Naturvetenskapliga fakulteten, Institutionen för molekylär biovetenskap, Wenner-Grens institut. University Medical Center Hamburg-Eppendorf, Germany.
Stockholms universitet, Naturvetenskapliga fakulteten, Institutionen för molekylär biovetenskap, Wenner-Grens institut.
Stockholms universitet, Naturvetenskapliga fakulteten, Institutionen för molekylär biovetenskap, Wenner-Grens institut.
Stockholms universitet, Naturvetenskapliga fakulteten, Institutionen för molekylär biovetenskap, Wenner-Grens institut.
Visa övriga samt affilieringar
Antal upphovsmän: 52016 (Engelska)Ingår i: American Journal of Physiology. Endocrinology and Metabolism, ISSN 0193-1849, E-ISSN 1522-1555, Vol. 311, nr 1, s. e202-e213Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

The development of obesity may be aggravated if obesity itself insulates against heat loss and thus diminishes the amount of food burnt for body temperature control. This would be particularly important under normal laboratory conditions where mice experience a chronic cold stress (at approximate to 20 degrees C). We used Scholander plots (energy expenditure plotted against ambient temperature) to examine the insulation (thermal conductance) of mice, defined as the inverse of the slope of the Scholander curve at subthermoneutral temperatures. We verified the method by demonstrating that shaved mice possessed only half the insulation of non-shaved mice. We examined a series of obesity models [mice fed high-fat diets and kept at different temperatures, classical diet-induced obese mice, ob/ob mice, and obesity-prone (C57BL/6) vs. obesity-resistant (129S)mice]. We found that neither acclimation temperature nor any kind or degree of obesity affected the thermal insulation of the mice when analyzed at the whole mouse level or as energy expenditure per lean weight. Calculation per body weight erroneously implied increased insulation in obese mice. We conclude that, in contrast to what would be expected, obesity of any kind does not increase thermal insulation in mice, and therefore, it does not in itself aggravate the development of obesity. It may be discussed as to what degree of effect excess adipose tissue has on insulation in humans and especially whether significant metabolic effects are associated with insulation in humans.

Ort, förlag, år, upplaga, sidor
2016. Vol. 311, nr 1, s. e202-e213
Nyckelord [en]
obesity, insulation, ob/ob
Nationell ämneskategori
Biologiska vetenskaper Fysiologi
Forskningsämne
fysiologi
Identifikatorer
URN: urn:nbn:se:su:diva-133223DOI: 10.1152/ajpendo.00093.2016ISI: 000380372000016PubMedID: 27189935OAI: oai:DiVA.org:su-133223DiVA, id: diva2:970442
Tillgänglig från: 2016-09-13 Skapad: 2016-09-05 Senast uppdaterad: 2022-02-23Bibliografiskt granskad
Ingår i avhandling
1. Energy flow and metabolic efficiency attributed to brown adipose tissue
Öppna denna publikation i ny flik eller fönster >>Energy flow and metabolic efficiency attributed to brown adipose tissue
2017 (Engelska)Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
Abstract [en]

The large capacity of brown adipose tissue (BAT) to expend energy as heat makes it an interesting potential player in weight regulation and other metabolic conditions. This is of particular interest as it has been recognized that adult humans possess BAT. The protein responsible for the heat production is uncoupling protein 1 (UCP1), which, as the name implies, uncouples the respiratory chain from ATP production; instead heat is produced. Cold is the strongest recruiter and activator of BAT. However, also obesogenic food has a low but nonetheless significant effect on the recruitment and activation of UCP1, although the significance of this has been discussed.

In the present thesis, I have studied the effect of diet on BAT and the possibilities for it to be obesity-protective. This can be done by comparing responses in wild-type mice and in UCP1-ablated mice. Since the effect of diet on BAT is low, it is of importance to control the temperature and maintain thermoneutrality. Other confounding factors to keep in mind are differences in actual energy and composition of food and also cohort differences. When controlling all the parameters mentioned and giving the mice the same obesogenic diet, the mice possessing UCP1 compared to UCP1-ablated mice had higher energy expenditure, and lower weight gain, despite eating more. This confirms the presence of a UCP1-dependent diet-induced thermogenesis. Thus, the conclusion must be that possessing UCP1 does result in obesity protection at thermoneutrality. However, the relevance for human energy balance is still not established.

Ort, förlag, år, upplaga, sidor
Stockholm: Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, 2017. s. 86
Nyckelord
Brown adipose tissue, BAT, UCP1, diet-induced thermogenesis, DIT, obesity, high-fat diet, energy expenditure
Nationell ämneskategori
Fysiologi
Forskningsämne
fysiologi
Identifikatorer
urn:nbn:se:su:diva-140190 (URN)978-91-7649-734-0 (ISBN)978-91-7649-735-7 (ISBN)
Disputation
2017-04-07, Vivi Täckholmsalen (Q-salen), NPQ-huset, Svante Arrhenius väg 20, Stockholm, 10:00 (Engelska)
Opponent
Handledare
Anmärkning

At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 1: Manuscript. Paper 2: Manuscript. Paper 3: Manuscript.

Tillgänglig från: 2017-03-15 Skapad: 2017-03-07 Senast uppdaterad: 2022-02-28Bibliografiskt granskad

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Fischer, Alexander W.Csikasz, Robert I.von Essen, GabriellaCannon, BarbaraNedergaard, Jan

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Fischer, Alexander W.Csikasz, Robert I.von Essen, GabriellaCannon, BarbaraNedergaard, Jan
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American Journal of Physiology. Endocrinology and Metabolism
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