Short-term cooling increases serum triglycerides and small high-density lipoprotein levels in humans

Hoeke, Geerte; Nahon, Kimberly J.; Bakker, Leontine E. H.; Norkauer, Sabine; Dinnes, Donna Lee M.; Kockx, Maaike; Lichtenstein, Laeticia; Drettwan, Diana; Reifel‐Miller, Anne; Coşkun, Tamer; Pagel, Philipp; Romijn, Fred P.H.T.M.; Cobbaert, Christa; Jazet, Ingrid M.; Martinez, Laurent O.; Kritharides, Leonard; Berbée, Jimmy F.P.; Boon, Mariëtte R.; Rensen, Patrick C.N.

doi:10.1016/j.jacl.2017.04.117

Cited by 37 publications

(47 citation statements)

References 35 publications

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“…As can be expected from stimulation of the sympathetic system activity, acute cold exposure leads to robust increase in plasma NEFA levels and appearance rate ( 39 , 108 , 109 , 141 ). Upregulation of genes of lipid utilization was shown in BAT with cold exposure in humans ( 134 ).…”

Section: Energy Substrates Utilization By Batmentioning

confidence: 74%

Brown Adipose Tissue Energy Metabolism in Humans

et al. 2018

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The demonstration of metabolically active brown adipose tissue (BAT) in humans primarily using positron emission tomography coupled to computed tomography (PET/CT) with the glucose tracer 18-fluorodeoxyglucose (18FDG) has renewed the interest of the scientific and medical community in the possible role of BAT as a target for the prevention and treatment of obesity and type 2 diabetes (T2D). Here, we offer a comprehensive review of BAT energy metabolism in humans. Considerable advances in methods to measure BAT energy metabolism, including nonesterified fatty acids (NEFA), chylomicron-triglycerides (TG), oxygen, Krebs cycle rate, and intracellular TG have led to very good quantification of energy substrate metabolism per volume of active BAT in vivo. These studies have also shown that intracellular TG are likely the primary energy source of BAT upon activation by cold. Current estimates of BAT's contribution to energy expenditure range at the lower end of what would be potentially clinically relevant if chronically sustained. Yet, 18FDG PET/CT remains the gold-standard defining method to quantify total BAT volume of activity, used to calculate BAT's total energy expenditure. Unfortunately, BAT glucose metabolism better reflects BAT's insulin sensitivity and blood flow. It is now clear that most glucose taken up by BAT does not fuel mitochondrial oxidative metabolism and that BAT glucose uptake can therefore be disconnected from thermogenesis. Furthermore, BAT thermogenesis is efficiently recruited upon repeated cold exposure, doubling to tripling its total oxidative capacity, with reciprocal reduction of muscle thermogenesis. Recent data suggest that total BAT volume may be much larger than the typically observed 50–150 ml with 18FDG PET/CT. Therefore, the current estimates of total BAT thermogenesis, largely relying on total BAT volume using 18FDG PET/CT, may underestimate the true contribution of BAT to total energy expenditure. Quantification of the contribution of BAT to energy expenditure begs for the development of more integrated whole body in vivo methods.

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Section: Energy Substrates Utilization By Batmentioning

confidence: 74%

Brown Adipose Tissue Energy Metabolism in Humans

et al. 2018

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“…Vallerand and Jacobs () report that acute cold exposure triggers an increase in lipid oxidation of 63% and an increase in carbohydrate oxidation of 588%. Two hours of mild cooling is associated with an increase in small LDL and HDL particles (Hoeke et al, ). In a transgenic mouse model of dyslipidemia, thermogenic adipocytes exposed to cold stress exhibit accelerated plasma cholesterol efflux and fecal excretion (Bartelt et al, ).…”

Section: Discussionmentioning

confidence: 99%

Brown adipose tissue, energy expenditure, and biomarkers of cardio‐metabolic health among the Yakut (Sakha) of northeastern Siberia

Lévy

Климова

Zakharova

et al. 2018

American J Hum Biol

105

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Objectives: This study provides the first investigation of non-shivering thermogenesis (NST) and brown adipose tissue (BAT) activity among an indigenous circumpolar population, the Yakut of northeastern Siberia. The study also examines the health significance of BAT activity in this population by testing the relationships between BAT thermogenesis and biomarkers of cardio-metabolic disease risk, such as percent body fat and blood glucose and cholesterol levels. Methods: Data were collected in the Sakha Republic (Yakutia) for 31 men and 43 women. Change in energy expenditure and BAT thermogenesis were quantified after a 30-minute mild cooling condition. Anthropometric dimensions, blood glucose, and lipid levels were also collected. Results: On average, the skin temperature of the supraclavicular area was constant after cooling while the skin temperature of a point on the sternum dropped significantly (P < .001), thus suggesting the presence of active supraclavicular BAT among Yakut adults. Participants with evidence of greater BAT thermogenesis exhibited a larger percent change in energy expenditure (% ΔEE) and an increase in respiratory quotient (RQ) after cooling (P ≤ .05). While there was no relationship between BAT activity and blood lipid levels, BAT thermogenesis was positively associated with blood glucose levels (P < .01). Conclusions: Yakut adults exhibit evidence of active BAT deposits. Given that there is a significant relationship between BAT activity and % ΔEE, it is possible that BAT plays a role in NST among Yakut adults. While the relationship between BAT and body composition is inconclusive, participants with greater BAT seemed to preferentially utilize glucose during cold stress exposure.

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“…The lipoprotein analysis was conducted via deconvolution of the broad methyl group signal at about 0.9–0.8 ppm. The concentrations of lipoprotein particles and cholesterol in lipoprotein (sub‐)classes as well as the average particle size (23 lipoprotein‐related parameters in total) were calculated based on the integrals attributable to specific base functions and underwent statistical evaluation . All the measured lipid parameters are given: concentration of large very low‐density lipoprotein (VLDL) particles (LVLDL‐P), of LDL‐P, of large LDL particles (LLDL‐P), of small LDL particles (SLDL‐P), of HDL particles (HDL‐P), of large HDL particles (LHDL‐P), of small HDL particles (SHDL‐P); mean size of VLDL particles (VLDL‐s), of LDL‐P (LDL‐s), of HDL‐P (HDL‐s); cholesterol concentration in VLDL class (VLDL‐c), in intermediate‐density lipoprotein (IDL) class (IDL‐c), in LDL class (LDL‐c), in LDL subclass A (large particles) (LDL.A‐c), in LDL subclass B (medium‐sized particles) (LDL.B‐c), in LDL subclass A (small particles) (LDL.C‐c), in HDL subclass A (large particles) (HDL.A‐c), in HDL subclass B (medium‐sized particles) (HDL.B‐c), in HDL subclass A (small particles) (HDL.C‐c), total cholesterol, LDL‐cholesterol, HDL‐cholesterol, and triglycerides.…”

Section: Methodsmentioning

confidence: 99%

“…The lipoprotein analysis was conducted via deconvolution of the broad methyl group signal at about 0.9-0.8 ppm. The concentrations of lipoprotein particles and cholesterol in lipoprotein (sub-)classes as well as the average particle size (23 lipoproteinrelated parameters in total) were calculated based on the integrals attributable to specific base functions and underwent statistical evaluation (13). All the measured lipid parameters are given: concentration of large very low-density lipoprotein (VLDL) particles (LVLDL-P), of LDL-P, of large LDL particles (LLDL-P), of small LDL particles (SLDL-P), Table 2, when statistical changes could be determined between the four groups.…”

Section: Lipoprotein Profilingmentioning

confidence: 99%

NMR‐based lipoprotein analysis for patients with severe hypercholesterolemia undergoing lipoprotein apheresis or PCSK9‐inhibitor therapy (NAPALI‐Study)

Schettler¹,

Muellendorff²,

Schettler³

et al. 2019

Ther Apher Dial

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Taking into account the discordance between low‐density lipoprotein cholesterol (LDL‐C) and LDL particle (LDL‐P) number, cardiovascular risk more closely correlates with LDL‐P in patients. The aim of our study was to evaluate the number of lipid particles in patients with severe hypercholesterolemia treated with different lipid‐lowering regimens. Four groups of patients differing with respect to lipid‐lowering therapy were recruited from hypercholesterolemic outpatients and lipoprotein apheresis (LA) facilities, and were treated with statins alone (group A), with statins and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors (PCSK9i) (group B), with statins and LA (group C), or with statins, PCSK9i, and LA (group D). Cholesterol, triglycerides, LDL‐C, high‐density lipoprotein cholesterol (HDL‐C), LDL‐P number and size, HDL‐P number and size were determined using nuclear magnetic resonance spectroscopy. The lowest LDL‐P number was achieved at the end of LA sessions in combination with statins or in combination with statins and a monoclonal PCSK9i (median; 25th and 75th percentile) (group C: 244 nmoL/L: 237, 244, P < 0.05; group D: 244 nmoL/L: 99, 307, P < 0.05). Comparing LDL‐P number at the start of LA (group C: 978 nmoL/L: 728, 1404; group D: 954 nmoL/L: 677, 1521) to the other patient groups (groups A and B), the lowest LDL‐P number was measured in patients treated with PCSK9i and a statin (group B): LDL‐P (762 nmoL/L: 604, 1043, P < 0.05), large LDL‐P (472 nmoL/L: 296, 574, P < 0.05), and small LDL‐P (342 nmoL/L: 152, 494, P < 0.05). Very low‐density lipoprotein and HDL particle sizes remained approximately the same in all groups. LA in combination with statins or in combination with statins and PCSK9i most reduced LDL‐P numbers in hypercholesterolemic patients.

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Short-term cooling increases serum triglycerides and small high-density lipoprotein levels in humans

Cited by 37 publications

References 35 publications

Brown Adipose Tissue Energy Metabolism in Humans

Brown Adipose Tissue Energy Metabolism in Humans

Brown adipose tissue, energy expenditure, and biomarkers of cardio‐metabolic health among the Yakut (Sakha) of northeastern Siberia

NMR‐based lipoprotein analysis for patients with severe hypercholesterolemia undergoing lipoprotein apheresis or PCSK9‐inhibitor therapy (NAPALI‐Study)

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