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Shabalina, I., Edgar, D., Gibanova, N., Kalinovich, A., Petrovic, N., Vyssokikh, M. Y., . . . Nedergaard, J. (2024). Enhanced ROS Production in Mitochondria from Prematurely Aging mtDNA Mutator Mice. Biochemistry (Moscow), 89(2), 279-298
Åpne denne publikasjonen i ny fane eller vindu >>Enhanced ROS Production in Mitochondria from Prematurely Aging mtDNA Mutator Mice
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2024 (engelsk)Inngår i: Biochemistry (Moscow), ISSN 0006-2979, E-ISSN 1608-3040, Vol. 89, nr 2, s. 279-298Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

An increase in mitochondrial DNA (mtDNA) mutations and an ensuing increase in mitochondrial reactive oxygen species (ROS) production have been suggested to be a cause of the aging process (the mitochondrial hypothesis of aging). In agreement with this, mtDNA-mutator mice accumulate a large amount of mtDNA mutations, giving rise to defective mitochondria and an accelerated aging phenotype. However, incongruously, the rates of ROS production in mtDNA mutator mitochondria have generally earlier been reported to be lower - not higher - than in wildtype, thus apparently invalidating the mitochondrial hypothesis of aging. We have here re-examined ROS production rates in mtDNA-mutator mice mitochondria. Using traditional conditions for measuring ROS (succinate in the absence of rotenone), we indeed found lower ROS in the mtDNA-mutator mitochondria compared to wildtype. This ROS mainly results from reverse electron flow driven by the membrane potential, but the membrane potential reached in the isolated mtDNA-mutator mitochondria was 33 mV lower than that in wildtype mitochondria, due to the feedback inhibition of succinate oxidation by oxaloacetate, and to a lower oxidative capacity in the mtDNA-mutator mice, explaining the lower ROS production. In contrast, in normal forward electron flow systems (pyruvate (or glutamate) + malate or palmitoyl-CoA + carnitine), mitochondrial ROS production was higher in the mtDNA-mutator mitochondria. Particularly, even during active oxidative phosphorylation (as would be ongoing physiologically), higher ROS rates were seen in the mtDNA-mutator mitochondria than in wildtype. Thus, when examined under physiological conditions, mitochondrial ROS production rates are indeed increased in mtDNA-mutator mitochondria. While this does not prove the validity of the mitochondrial hypothesis of aging, it may no longer be said to be negated in this respect. This paper is dedicated to the memory of Professor Vladimir P. Skulachev.

Emneord
mtDNA mutator mice, ROS production, aging, succinate, membrane potential, oxidative phosphorylation
HSV kategori
Identifikatorer
urn:nbn:se:su:diva-228605 (URN)10.1134/S0006297924020081 (DOI)001190797800013 ()38622096 (PubMedID)2-s2.0-85188236462 (Scopus ID)
Tilgjengelig fra: 2024-04-23 Laget: 2024-04-23 Sist oppdatert: 2024-04-23bibliografisk kontrollert
Nedergaard, J., von Essen, G. & Cannon, B. (2023). Brown adipose tissue: can it keep us slim? A discussion of the evidence for and against the existence of diet-induced thermogenesis in mice and men. Philosophical Transactions of the Royal Society of London. Biological Sciences, 378(1888), Article ID 20220220.
Åpne denne publikasjonen i ny fane eller vindu >>Brown adipose tissue: can it keep us slim? A discussion of the evidence for and against the existence of diet-induced thermogenesis in mice and men
2023 (engelsk)Inngår i: Philosophical Transactions of the Royal Society of London. Biological Sciences, ISSN 0962-8436, E-ISSN 1471-2970, Vol. 378, nr 1888, artikkel-id 20220220Artikkel, forskningsoversikt (Fagfellevurdert) Published
Abstract [en]

The issue under discussion here is whether a decrease in the degree of UCP1 activity (and brown adipose tissue activity in general) could be a cause of obesity in humans. This possibility principally requires the existence of the phenomenon of diet-induced thermogenesis. Obesity could be a consequence of a reduced functionality of diet-induced thermogenesis. Experiments in mice indicate that diet-induced thermogenesis exists and is dependent on the presence of UCP1 and thus of brown adipose tissue activity. Accordingly, many (but not all) experiments indicate that in the absence of UCP1, mice become obese. Whether similar mechanisms exist in humans is still unknown. A series of studies have indicated a correlation between obesity and low brown adipose tissue activity, but it may be so that the obesity itself may influence the estimates of brown adipose tissue activity (generally glucose uptake), partly explaining the relationship. Estimates of brown adipose tissue catabolizing activity would seem to indicate that it may possess a capacity sufficient to help maintain body weight, and obesity would thus be aggravated in its absence.

Emneord
diet-induced thermogenesis, UCP1, brown adipose tissue
HSV kategori
Identifikatorer
urn:nbn:se:su:diva-222198 (URN)10.1098/rstb.2022.0220 (DOI)001062424100013 ()37661736 (PubMedID)2-s2.0-85169651199 (Scopus ID)
Tilgjengelig fra: 2023-10-17 Laget: 2023-10-17 Sist oppdatert: 2023-10-17bibliografisk kontrollert
Galvão Valdivia, L. F., Castro, É., dos Santos Eichler, R. A., Moreno, M. F., de Sousa, É., Rodrigues Jardim, G. F., . . . Reckziegel, P. (2023). Cold acclimation and pioglitazone combined increase thermogenic capacity of brown and white adipose tissues but this does not translate into higher energy expenditure in mice. American Journal of Physiology. Endocrinology and Metabolism, 324(4), E358-E373
Åpne denne publikasjonen i ny fane eller vindu >>Cold acclimation and pioglitazone combined increase thermogenic capacity of brown and white adipose tissues but this does not translate into higher energy expenditure in mice
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2023 (engelsk)Inngår i: American Journal of Physiology. Endocrinology and Metabolism, ISSN 0193-1849, E-ISSN 1522-1555, Vol. 324, nr 4, s. E358-E373Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Cold acclimation and pharmacological peroxisome proliferator-activated receptor γ (PPARγ) activation have each earlier been shown to recruit brown adipose tissue (BAT) and beige adipocytes thermogenic machinery, enhancing uncoupling protein 1 (UCP1)-mediated thermogenic capacity. We here investigated whether cold acclimation and PPARγ agonism combined have additive effects in inducing brown and beige adipocytes UCP1 content and whether this translates into a higher thermogenic capacity and energy expenditure. C57BL/6J mice treated or not with pioglitazone (30 mg/kg/day) were maintained at 21°C or exposed to cold (7°C) for 15 days and evaluated for thermogenic capacity, energy expenditure and interscapular BAT (iBAT) and inguinal white adipose tissue (iWAT) mass, morphology, UCP1 content and gene expression, glucose uptake and oxygen consumption. Cold acclimation and PPARγ agonism combined synergistically increased iBAT and iWAT total UCP1 content and mRNA levels of the thermogenesis-related proteins PGC1a, CIDEA, FABP4, GYK, PPARa, LPL, GLUTs (GLUT1 in iBAT and GLUT4 in iWAT), and ATG when compared to cold and pioglitazone individually. This translated into a stronger increase in body temperature in response to the β3-adrenergic agonist CL316,243 and iBAT and iWAT respiration induced by succinate and pyruvate in comparison to that seen in either cold-acclimated or pioglitazone-treated mice. However, basal energy expenditure, BAT glucose uptake and glucose tolerance were not increased above that seen in cold-acclimated untreated mice. In conclusion, cold acclimation and PPARγ agonism combined induced a robust increase in brown and beige adipocytes UCP1 content and thermogenic capacity, much higher than each treatment individually. However, our findings enforce the concept that increases in total UCP1 do not innately lead to higher energy expenditure.

Emneord
adipogenesis, browning, pioglitazone, thermogenesis, UCP1
HSV kategori
Identifikatorer
urn:nbn:se:su:diva-216979 (URN)10.1152/ajpendo.00217.2022 (DOI)000974585600001 ()36856189 (PubMedID)2-s2.0-85152170431 (Scopus ID)
Tilgjengelig fra: 2023-05-09 Laget: 2023-05-09 Sist oppdatert: 2023-05-09bibliografisk kontrollert
von Essen, G., Lindsund, E., Maldonado, E., Zouhar, P., Cannon, B. & Nedergaard, J. (2023). Highly recruited brown adipose tissue does not in itself protect against obesity. Molecular Metabolism, 76, Article ID 101782.
Åpne denne publikasjonen i ny fane eller vindu >>Highly recruited brown adipose tissue does not in itself protect against obesity
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2023 (engelsk)Inngår i: Molecular Metabolism, ISSN 2212-8778, Vol. 76, artikkel-id 101782Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Objective: The possibility to counteract the development of obesity in humans by recruiting brown or brite/beige adipose tissue (and thus UCP1) has attracted much attention. Here we examine if a diet that can activate diet-induced thermogenesis can exploit pre-enhanced amounts of UCP1 to counteract the development of diet-induced obesity.Methods: To investigate the anti-obesity significance of highly augmented amounts of UCP1 for control of body energy reserves, we physiologically increased total UCP1 amounts by recruitment of brown and brite/beige tissues in mice. We then examined the influence of the augmented UCP1 levels on metabolic parameters when the mice were exposed to a high-fat/high-sucrose diet under thermoneutral conditions.Results: The total UCP1 levels achieved were about 50-fold higher in recruited than in non-recruited mice. Contrary to underlying expectations, in the mice with highly recruited UCP1 and exposed to a high-fat/high-sucrose diet the thermogenic capacity of this UCP1 was completely inactivate. The mice even transiently (in an adipostat-like manner) demonstrated a higher metabolic efficiency and fat gain than did non-recruited mice. This was accomplished without altering energy expenditure or food absorption efficiency. The metabolic efficiency here was indistinguishable from that of mice totally devoid of UCP1.Conclusions: Although UCP1 protein may be available, it is not inevitably utilized for diet-induced thermogenesis. Thus, although attempts to recruit UCP1 in humans may become successful as such, it is only if constant activation of the UCP1 is also achieved that amelioration of obesity development could be attained.& COPY; 2023 The Authors. Published by Elsevier GmbH. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

Emneord
Diet-induced thermogenesis, UCP1, Body weight regulation, Beige adipose tissue, Adipostat, Glucose homeostasis
HSV kategori
Identifikatorer
urn:nbn:se:su:diva-222230 (URN)10.1016/j.molmet.2023.101782 (DOI)001063640000001 ()37499977 (PubMedID)2-s2.0-85167813527 (Scopus ID)
Tilgjengelig fra: 2023-10-11 Laget: 2023-10-11 Sist oppdatert: 2023-10-11bibliografisk kontrollert
Nedergaard, J., Fischer, A. W. & Cannon, B. (2023). Leptin as an Antitorpor Hormone: An Explanation for the Increased Metabolic Efficiency and Cold Sensitivity of ob/ob Mice?. Physiological and Biochemical Zoology, 96(1), 30-39
Åpne denne publikasjonen i ny fane eller vindu >>Leptin as an Antitorpor Hormone: An Explanation for the Increased Metabolic Efficiency and Cold Sensitivity of ob/ob Mice?
2023 (engelsk)Inngår i: Physiological and Biochemical Zoology, ISSN 1522-2152, E-ISSN 1537-5293, Vol. 96, nr 1, s. 30-39Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Leptin is recognized as an anorexigenic hormone. In its absence (e.g., in ob/ob mutant mice), mice become obese, primarily as a result of hyperphagia. A recurrent question is whether, additionally, leptin is thermogenic and thus also an antiobesity hormone in this way. We have earlier reviewed available data and have concluded that most articles implying a thermogenic effect of leptin have based this on a misconstrued division by body weight. Here, we have collected evidence that the remaining observations that imply that leptin is a thermogenic hormone are better understood as implying that leptin is an antitorpor hormone. Leptin levels increase in proportion to the body's energy reserves (i.e., stored lipids in the adipose tissue), and leptin thus serves as an indicator of energy availability. In the absence of leptin, ob/ob mice are exceedingly prone to enter daily torpor, since the absence of leptin causes them to perceive a lack of body energy reserves that, in combination with restricted or no food, induces them to enter the torpid state to save energy. This antitorpor effect of leptin probably explains the following earlier observations. First, ob/ob mice have the ability to gain weight even when pair fed with leptin-treated ob/ob mice. This is understood as follows: In the leptin-treated ob/ob mice, food intake is reduced. Untreated pair-fed mice enter daily torpor, and this markedly lowers total daily energy expenditure; the resulting surplus food energy is then accumulated as fat in these mice. However, ob/ob mice fed ad lib. do not enter torpor, so under normal conditions this mechanism does not contribute to the obesity found in the ob/ob mice. Second, neonatal ob/ob mice have the ability to become obese despite eating the same amount as wild-type mice: this is understood as these mice similarly entering daily torpor. Third, ob/ob mice on the C57BL/6J background have a lower metabolic rate: these mice were examined in the absence of food, and torpor was thus probably induced. Fourth, ob/ob mice have apparent high cold sensitivity: these mice experienced cold in the absence of food and would immediately enter deep torpor. It is suggested that this novel explanation of how the antitorpor effects of leptin affect mouse energy metabolism can open new avenues for leptin research.

Emneord
torpor, ob/ob mice, leptin, thermogenesis
HSV kategori
Identifikatorer
urn:nbn:se:su:diva-223184 (URN)10.1086/722135 (DOI)001072870100003 ()36626840 (PubMedID)2-s2.0-85145369976 (Scopus ID)
Tilgjengelig fra: 2023-10-26 Laget: 2023-10-26 Sist oppdatert: 2023-10-26bibliografisk kontrollert
Davies, V. S., Lindsund, E., Petrovic, N., Cannon, B. & Nedergaard, J. (2023). Repeated short excursions from thermoneutrality suffice to restructure brown adipose tissue. Biochimie, 210, 40-49
Åpne denne publikasjonen i ny fane eller vindu >>Repeated short excursions from thermoneutrality suffice to restructure brown adipose tissue
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2023 (engelsk)Inngår i: Biochimie, ISSN 0300-9084, E-ISSN 1638-6183, Vol. 210, s. 40-49Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Given the presence of brown adipose tissue in adult humans, an important issue is whether human brown adipose tissue is recruitable. Cold exposure is the canonical recruitment treatment; however, in experimental animals (mice), recruitment of brown adipose tissue is normally induced by placing the mice in constant cold, a procedure not feasible in humans. For possible translational applications, we have therefore investigated whether shorter daily excursions from thermoneutrality would suffice to qualitatively and quantitatively induce recruitment in mice. Mice, housed at thermoneutrality (30 °C) to mimic human conditions, were transferred every day for 4 weeks to cool conditions (18 °C), for 0, 15, 30, 120 and 420 min (or placed constantly in 18 °C). On the examination day, the mice were not exposed to cold. Very short daily exposures (≤30 minutes) were sufficient to induce structural changes in the form of higher protein density in brown adipose tissue, changes that may affect the identification of the tissue in e.g. computer tomography and other scan studies. To estimate thermogenic capacity, UCP1 protein levels were followed. No UCP1 protein was detectable in inguinal white adipose tissue. In the interscapular brown adipose tissue, a remarkable two-phase reaction was seen. Very short daily exposures (≤30 minutes) were sufficient to induce a significant increase in total UCP1 levels. For attainment of full cold acclimation, the mice had, however, to remain exposed to the cold. The studies indicate that marked alterations in brown adipose tissue composition can be induced in mammals through relatively modest stimulation events.

HSV kategori
Identifikatorer
urn:nbn:se:su:diva-214074 (URN)10.1016/j.biochi.2023.01.006 (DOI)36657658 (PubMedID)2-s2.0-85148701823 (Scopus ID)
Tilgjengelig fra: 2023-01-23 Laget: 2023-01-23 Sist oppdatert: 2023-10-12bibliografisk kontrollert
Nedergaard, J. & Cannon, B. (2022). Diet-Induced Thermogenesis: Principles and Pitfalls. In: David A. Guertin, Christian Wolfrum (Ed.), Brown Adipose Tissue: Methods and Protocols (pp. 177-202). New York: Humana Press
Åpne denne publikasjonen i ny fane eller vindu >>Diet-Induced Thermogenesis: Principles and Pitfalls
2022 (engelsk)Inngår i: Brown Adipose Tissue: Methods and Protocols / [ed] David A. Guertin, Christian Wolfrum, New York: Humana Press, 2022, s. 177-202Kapittel i bok, del av antologi (Fagfellevurdert)
Abstract [en]

Concerning diet-induced thermogenesis, methodological issues relate mainly to the interpretation of measurements, rather than to the technical methodology as such. In the following, we point to a series of issues where the analysis often suggests the occurrence of UCP1-related diet-induced thermogenesis but where the observations are often the consequences of a process that has induced leanness rather than being the cause of them. We particularly emphasize the necessity of focusing on the total organism when interpreting biochemical and molecular data, where the concept of total tissue values rather than relative data better reflects physiologically important alterations. We stress the importance of performing experiments at thermoneutrality in order to obtain clinically relevant data and stress that true thermogenic agents may be overlooked if this is not done. 

sted, utgiver, år, opplag, sider
New York: Humana Press, 2022
Serie
Methods in Molecular Biology, ISSN 1064-3745, E-ISSN 1940-6029
Emneord
UCP1, Thermogenesis, Diet-induced thermogenesis, Metabolic efficiency
HSV kategori
Identifikatorer
urn:nbn:se:su:diva-204948 (URN)10.1007/978-1-0716-2087-8_12 (DOI)35167098 (PubMedID)2-s2.0-85124636688 (Scopus ID)978-1-0716-2086-1 (ISBN)978-1-0716-2087-8 (ISBN)
Tilgjengelig fra: 2022-05-23 Laget: 2022-05-23 Sist oppdatert: 2022-05-23bibliografisk kontrollert
Gao, Y., Shabalina, I. G., Braz, G. R., Cannon, B., Yang, G. & Nedergaard, J. (2022). Establishing the potency of N-acyl amino acids versus conventional fatty acids as thermogenic uncouplers in cells and mitochondria from different tissues. Biochimica et Biophysica Acta - Bioenergetics, 1863(4), Article ID 148542.
Åpne denne publikasjonen i ny fane eller vindu >>Establishing the potency of N-acyl amino acids versus conventional fatty acids as thermogenic uncouplers in cells and mitochondria from different tissues
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2022 (engelsk)Inngår i: Biochimica et Biophysica Acta - Bioenergetics, ISSN 0005-2728, E-ISSN 1879-2650, Vol. 1863, nr 4, artikkel-id 148542Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

The possibility that N-acyl amino acids could function as brown or brite/beige adipose tissue-derived lipokines that could induce UCP1-independent thermogenesis by uncoupling mitochondrial respiration in several peripheral tissues is of significant physiological interest. To quantify the potency of N-acyl amino acids versus conventional fatty acids as thermogenic inducers, we have examined the affinity and efficacy of two pairs of such compounds: oleate versus N-oleoyl-leucine and arachidonate versus N-arachidonoyl-glycine in cells and mitochondria from different tissues. We found that in cultures of the muscle-derived L6 cell line, as well as in primary cultures of murine white, brite/beige and brown adipocytes, the N-acyl amino acids were proficient uncouplers but that they did not systematically display higher affinity or potency than the conventional fatty acids, and they were not as efficient uncouplers as classical protonophores (FCCP). Higher concentrations of the N-acyl amino acids (as well as of conventional fatty acids) were associated with signs of deleterious effects on the cells. In liver mitochondria, we found that the N-acyl amino acids uncoupled similarly to conventional fatty acids, thus apparently via activation of the adenine nucleotide transporter-2. In brown adipose tissue mitochondria, the N-acyl amino acids were able to activate UCP1, again similarly to conventional fatty acids. We thus conclude that the formation of the acyl-amino acid derivatives does not confer upon the corresponding fatty acids an enhanced ability to induce thermogenesis in peripheral tissues, and it is therefore unlikely that the N-acyl amino acids are of specific physiological relevance as UCP1-independent thermogenic compounds.

Emneord
Adenine nucleotide transporter, Fatty acids, N-acyl amino acids, Nonshivering thermogenesis, Uncoupling protein-1, N-oleoyl-leu, N-arachidonoyl-gly
HSV kategori
Identifikatorer
urn:nbn:se:su:diva-204413 (URN)10.1016/j.bbabio.2022.148542 (DOI)000781771000002 ()35192808 (PubMedID)
Tilgjengelig fra: 2022-05-04 Laget: 2022-05-04 Sist oppdatert: 2022-05-04bibliografisk kontrollert
Cannon, B. & Nedergaard, J. (2021). A PERKy way to make mitochondrial cristae. Trends in endocrinology and metabolism, 32(7), 417-419
Åpne denne publikasjonen i ny fane eller vindu >>A PERKy way to make mitochondrial cristae
2021 (engelsk)Inngår i: Trends in endocrinology and metabolism, ISSN 1043-2760, E-ISSN 1879-3061, Vol. 32, nr 7, s. 417-419Artikkel, forskningsoversikt (Fagfellevurdert) Published
Abstract [en]

PERK protein, that is canonically associated with the response to endoplasmic reticulum stress, may be acquiring a new role as a regulator of the growth of mitochondrial cristae. This role is pertinent not only to the recruitment of brown adipose tissue thermogenic capacity but probably also to directing cristae formation in highly metabolically active organs such as the heart.

Emneord
brown adipose tissue, cristae, endoplasmic reticulum stress, MICOS, mitochondria, norepinephrine
HSV kategori
Identifikatorer
urn:nbn:se:su:diva-216147 (URN)10.1016/j.tem.2021.04.003 (DOI)000659494900002 ()33952415 (PubMedID)2-s2.0-85105358081 (Scopus ID)
Tilgjengelig fra: 2023-04-05 Laget: 2023-04-05 Sist oppdatert: 2023-04-05bibliografisk kontrollert
Zouhar, P., Janovska, P., Stanic, S., Bardova, K., Funda, J., Haberlova, B., . . . Nedergaard, J. (2021). A pyrexic effect of FGF21 independent of energy expenditure and UCP1. Molecular Metabolism, 53, Article ID 101324.
Åpne denne publikasjonen i ny fane eller vindu >>A pyrexic effect of FGF21 independent of energy expenditure and UCP1
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2021 (engelsk)Inngår i: Molecular Metabolism, ISSN 2212-8778, Vol. 53, artikkel-id 101324Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Objective: Administration of FGF21 to mice reduces body weight and increases body temperature. The increase in body temperature is generally interpreted as hyperthermia, i.e. a condition secondary to the increase in energy expenditure (heat production). Here, we examine an alternative hypothesis: that FGF21 has a direct pyrexic effect, i.e. FGF21 increases body temperature independently of any effect on energy expenditure.

Methods: We studied the effects of FGF21 treatment on body temperature and energy expenditure in high-fat-diet-fed and chow-fed mice exposed acutely to various ambient temperatures, in high-fat diet-fed mice housed at 30 °C (i.e. at thermoneutrality), and in mice lacking uncoupling protein 1 (UCP1).

Results: In every model studied, FGF21 increased body temperature, but energy expenditure was increased only in some models. The effect of FGF21 on body temperature was more (not less, as expected in hyperthermia) pronounced at lower ambient temperatures. Effects on body temperature and energy expenditure were temporally distinct (daytime versus nighttime). FGF21 enhanced UCP1 protein content in brown adipose tissue (BAT); there was no measurable UCP1 protein in inguinal brite/beige adipose tissue. FGF21 increased energy expenditure through adrenergic stimulation of BAT. In mice lacking UCP1, FGF21 did not increase energy expenditure but increased body temperature by reducing heat loss, e.g. a reduced tail surface temperature.

Conclusion: The effect of FGF21 on body temperature is independent of UCP1 and can be achieved in the absence of any change in energy expenditure. Since elevated body temperature is a primary effect of FGF21 and can be achieved without increasing energy expenditure, only limited body weight-lowering effects of FGF21 may be expected.

Emneord
UCP1, Thermoneutrality, Beiging, browning, Obesity, Body temperature control
HSV kategori
Identifikatorer
urn:nbn:se:su:diva-198500 (URN)10.1016/j.molmet.2021.101324 (DOI)000702820300003 ()34418595 (PubMedID)
Tilgjengelig fra: 2021-11-11 Laget: 2021-11-11 Sist oppdatert: 2022-02-25bibliografisk kontrollert
Organisasjoner
Identifikatorer
ORCID-id: ORCID iD iconorcid.org/0000-0003-2070-1587