scholarly journals Paternal hyperglycemia in rats exacerbates the development of obesity in offspring

2017 ◽  
Vol 234 (2) ◽  
pp. 175-186 ◽  
Author(s):  
Xiaoqin Shi ◽  
Xinyu Li ◽  
Yi Hou ◽  
Xuemei Cao ◽  
Yuyao Zhang ◽  
...  
Keyword(s):  
Food Intake ◽  
Cold Exposure ◽  
Metabolic Diseases ◽  
Identical Condition ◽  
Female Rats ◽  
Normal Female ◽  
Citrate Buffer ◽  
Parental History ◽  
Leptin Signaling ◽  
Brown Adipose

Parental history with obesity or diabetes will increase the risk for developing metabolic diseases in offspring. However, literatures as to transgenerational inheritance of metabolic dysfunctions through male lineage are relatively scarce. In the current study, we aimed to evaluate influences of paternal hyperglycemia on metabolic phenotypes in offspring. Male SD rats were i.p. injected with streptozotocin (STZ) or citrate buffer (CB, as control). STZ-injected rats with glucose levels higher than 16.7 mM were selected to breed with normal female rats. Offspring from STZ or CB treated fathers (STZ-O and CB-O) were maintained in the identical condition. We monitored body weight and food intake, and tests of glucose and insulin tolerance (GTTs and ITTs), fasting–refeeding and cold exposure were performed. Expression of factors involved in hypothalamic feeding and brown adipose tissue (BAT) thermogenic activity was performed by real-time PCR and Western blot. Adult STZ-O were heavier than CB-O. Impairment of GTTs was observed in STZ-O compared with CB-O at 22 and 32 weeks of age; ITTs results showed decreased insulin sensitivity in STZ-O. Daily food intake and accumulated food intake during 12-h refeeding after fasting were significantly higher in STZ-O. UCP1 levels were downregulated in BAT from STZ-O at room temperature and cold exposure. Finally, STZ-O rats showed suppressed leptin signaling in the hypothalamus as evidenced by upregulated SOCS3, reduced phosphorylation of STAT3, impaired processing POMC and decreased α-MSH production. Our study revealed that paternal hyperglycemia predisposes offspring to developing obesity, which is possibly associated with impaired hypothalamic leptin signaling.

scholarly journals Deficiency of PTP1B in POMC neurons leads to alterations in energy balance and homeostatic response to cold exposure

2011 ◽  
Vol 300 (6) ◽  
pp. E1002-E1011 ◽  
Author(s):  
Bart C. De Jonghe ◽  
Matthew R. Hayes ◽  
Ryoichi Banno ◽  
Karolina P. Skibicka ◽  
Derek J. Zimmer ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Energy Balance ◽  
Food Intake ◽  
Cold Exposure ◽  
Tyrosine Phosphatase ◽  
Negative Regulator ◽  
Leptin Signaling ◽  
Leptin Sensitivity ◽  
Brown Adipose

The adipose tissue-derived hormone leptin regulates energy balance through catabolic effects on central circuits, including proopiomelanocortin (POMC) neurons. Leptin activation of POMC neurons increases thermogenesis and locomotor activity. Protein tyrosine phosphatase 1B (PTP1B) is an important negative regulator of leptin signaling. POMC neuron-specific deletion of PTP1B in mice results in reduced high-fat diet-induced body weight and adiposity gain due to increased energy expenditure and greater leptin sensitivity. Mice lacking the leptin gene ( ob/ob mice) are hypothermic and cold intolerant, whereas leptin delivery to ob/ob mice induces thermogenesis via increased sympathetic activity to brown adipose tissue (BAT). Here, we examined whether POMC PTP1B mediates the thermoregulatory response of CNS leptin signaling by evaluating food intake, body weight, core temperature (TC), and spontaneous physical activity (SPA) in response to either exogenous leptin or 4-day cold exposure (4°C) in male POMC-Ptp1b-deficient mice compared with wild-type controls. POMC-Ptp1b −/− mice were hypersensitive to leptin-induced food intake and body weight suppression compared with wild types, yet they displayed similar leptin-induced increases in TC. Interestingly, POMC-Ptp1b −/− mice had increased BAT weight and elevated plasma triiodothyronine (T3) levels in response to a 4-day cold challenge, as well as reduced SPA 24 h after cold exposure, relative to controls. These data show that PTP1B in POMC neurons plays a role in short-term cold-induced reduction of SPA and may influence cold-induced thermogenesis via enhanced activation of the thyroid axis.

scholarly journals Systematic assessment of lipid profiles for the discovery of tissue contributors to the circulating lipid pool in cold exposure

2021 ◽  
Author(s):  
Raghav Jain ◽  
Gina Wade ◽  
Irene Ong ◽  
Bhagirath Chaurasia ◽  
Judith Simcox
Keyword(s):  
Cold Exposure ◽  
Metabolic Diseases ◽  
Plasma Lipids ◽  
Acute Stress ◽  
Plasma Lipid ◽  
Functional Roles ◽  
Systematic Assessment ◽  
Lipid Pool ◽  
Brown Adipose

Plasma lipid levels are altered in chronic conditions such as type 2 diabetes and cardiovascular disease as well as acute stresses such as fasting and cold exposure. Advances in mass spectrometry based lipidomics have uncovered the complexity of the plasma lipidome which includes over 500 lipids that serve functional roles including energy substrate and signaling molecule. The plasma lipid pool is maintained through regulation of tissue production, secretion, and uptake. A major challenge is establishing the tissues of origin and uptake for various plasma lipids, which is necessary to determine the lipid function. Using cold exposure as an acute stress, we performed global lipidomics on the plasma and nine tissues that may contribute to the circulating pool. We found that numerous species of plasma acylcarnitines (ACars) and ceramides were significantly changed with cold exposure. Through computational assessment, we identified the liver and brown adipose tissue (BAT) as major contributors and consumers of circulating ACars, in agreement with our previous work. We further identified the kidney and intestine as novel contributors to the circulating ACar pool and validated these findings with gene expression analysis. Regression analysis also identified that the BAT and kidney as regulators of the plasma ceramide pool. These studies provide an adaptable computational tool to assess tissue contribution to the plasma lipid pool. Our findings have implications in understanding the function of plasma ACars and ceramides, which are elevated in metabolic diseases.

Effect of age and gender on thermoregulation

1989 ◽  
Vol 257 (4) ◽  
pp. R700-R704 ◽  
Author(s):  
R. B. McDonald ◽  
C. Day ◽  
K. Carlson ◽  
J. S. Stern ◽  
B. A. Horwitz
Keyword(s):  
Oxygen Consumption ◽  
Cold Exposure ◽  
Female Rats ◽  
Male Rats ◽  
Differential Heat ◽  
Independent Basis ◽  
Male And Female Rats ◽  
Brown Adipose ◽  
And Gender ◽  
Colonic Temperature

Previous investigations have shown that during cold exposure 24-mo-old male Fischer 344 (F344) rats do not thermoregulate as well as do 12-mo-old animals. To determine if this deficiency also occurs in female rats, we measured oxygen consumption (thermogenesis) and colonic temperature of male and female rats 5, 23, and 27 mo of age at rest and during 6 h of exposure to 6 degrees C. In addition, nonshivering thermogenesis (NST) was evaluated from the capacity of brown adipose tissue (BAT) mitochondria isolated from cold-exposed rats to bind guanosine 5'-diphosphate (GDP). Neither age nor gender had a significant effect on resting or cold-exposed oxygen consumption expressed on a mass-independent basis (l/kg body mass0.67) or on a lean body mass independent basis (l/kg lean body mass0.67). The drop in colonic temperature in response to cold was greater in the male rats. However, females exhibited increased BAT mass and relatively constant GDP binding with advancing age, whereas males showed decreased mass and GDP binding. Although the data suggest greater NST capacity in the female rats, rates of cold-induced oxygen consumption were similar in older female vs. male rats. Taken together, our data indicate that gender has a significant impact on thermoregulation and that, under the cold exposure conditions of the study, this effect involves differential heat conservation rather than heat production.

Restricted food intake limits brown adipose tissue hypertrophy in cold exposure

Life Sciences ◽  
1982 ◽  
Vol 30 (17) ◽  
pp. 1423-1426 ◽  
Author(s):  
T. Scott Johnson ◽  
Shawne Murray ◽  
James B. Young ◽  
Lewis Landsberg
Keyword(s):  
Adipose Tissue ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Brown Adipose ◽  
Restricted Food Intake

Effects of food and light on norepinephrine turnover

1988 ◽  
Vol 254 (5) ◽  
pp. R821-R827 ◽  
Author(s):  
T. Yoshida ◽  
G. A. Bray
Keyword(s):  
Food Intake ◽  
Ventromedial Hypothalamus ◽  
Female Rats ◽  
Light Cycle ◽  
Normal Cycle ◽  
Interscapular Brown Adipose Tissue ◽  
Male And Female Rats ◽  
Norepinephrine Turnover ◽  
Brown Adipose ◽  
Normal Light

To study diurnal differences in norepinephrine turnover, groups of rats were housed in rooms with alternating 12 h light and 12 h dark where half the animals were in a normal light cycle and half were in a reversed light cycle. Norepinephrine turnover was measured in all groups beginning at 1000 by inhibition of tyrosine hydroxylase. When rats are fed ad libitum, the turnover of norepinephrine in interscapular brown adipose tissue and heart was significantly higher in the normal cycle than in the reversed cycle. In addition, there was an interaction between the turnover of norepinephrine and the feeding and lighting schedules. When animals were adapted to eating from 0700 to 1900, the turnover of norepinephrine was somewhat faster when the animals ate in the reversed cycle than when they ate in the normal cycle. Conversely, when the feeding schedule was reversed and animals ate between 1900 and 0700, the turnover of norepinephrine in the absence of food was slightly slower in the animals eating in the reversed cycle than in those eating in the light cycle. This interaction between lighting and food intake observed in both male and female rats was abolished by ventromedial hypothalamic lesions. These data suggest that food intake and lighting conditions interact as controllers of the sympathetic nervous system and that these interactions are modulated by the ventromedial hypothalamus.

Insulin and metabolic efficiency in rats. II. Effects of NE and cold exposure

1986 ◽  
Vol 251 (6) ◽  
pp. R1118-R1125
Author(s):  
T. J. Bartness ◽  
C. J. Billington ◽  
A. S. Levine ◽  
J. E. Morley ◽  
N. E. Rowland ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Food Intake ◽  
Energy Expenditure ◽  
Cold Exposure ◽  
Diabetic Rats ◽  
Metabolic Efficiency ◽  
Maximal Energy ◽  
Brown Adipose

The role of insulin in metabolic efficiency (ME, i.e., efficiency of body wt gain) was examined under conditions of maximal energy expenditure in control and diabetic rats. Long-lasting insulin was administered using a protocol that did not affect food intake and increased ME in both groups. Half the animals were injected chronically with norepinephrine (NE). NE alone in controls decreased body weight and ME and increased brown adipose tissue (BAT) growth, thermogenic potential [cytochrome c oxidase activity (COA)], and lipoprotein lipases (LPL) activity; however, in diabetics, body weight, ME, and food intake all decreased and only BAT LPL activity and DNA content increased. The combination of NE and insulin increased BAT protein and COA in diabetics; in controls, all BAT measures were further increased and ME was intermediate to that of either treatment alone. Cold exposure decreased body weight and ME, increased food intake and qualitatively produced similar increases in BAT growth, COA, and LPL activity in both controls and diabetics. In diabetics, combined cold exposure and insulin did not affect the increase in BAT growth or LPL activity resulting from either treatment alone, but in controls this combination decreased BAT growth and COA. It is concluded that, even under conditions of maximal energy expenditure, both extremes of basal insulin status result in decreased BAT growth and thermogenic potential, but have opposite effects on ME.

scholarly journals Biomarkers of Browning in Cold Exposed Siberian Adults

Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2162
Author(s):  
Agrafena Efremova ◽  
Georgia Colleluori ◽  
Mikhail Thomsky ◽  
Jessica Perugini ◽  
Marina Protasoni ◽  
...  
Keyword(s):  
Cold Exposure ◽  
Mononuclear Cells ◽  
Metabolic Diseases ◽  
Exposed Group ◽  
Anthropometric Parameters ◽  
Cold Temperatures ◽  
Bat Activity ◽  
Fat Depots ◽  
Brown Adipose ◽  
White Fat

Cold-exposure promotes energy expenditure by inducing brown adipose tissue (BAT) thermogenesis, which over time, is also sustained by browning, the appearance, or increase, of brown-like cells into white fat depots. Identification of circulating markers reflecting BAT activity and browning is crucial to study this phenomenon and its triggers, also holding possible implications for the therapy of obesity and metabolic diseases. Using RT-qPCR, we evaluated the peripheral blood mononuclear cells (PBMC) expression profile of regulators of BAT activity (CIDEA, PRDM16), white adipocytes browning (HOXC9 and SLC27A1), and fatty acid β-oxidation (CPT1A) in 150 Siberian healthy miners living at extremely cold temperatures compared to 29 healthy subjects living in thermoneutral conditions. Anthropometric parameters, glucose, and lipid profiles were also assessed. The cold-exposed group showed significantly lower weight, BMI, hip circumference, and PBMC expression of CIDEA, but higher expression of HOXC9 and higher circulating glucose compared to controls. Within the cold-exposed group, BMI, total cholesterol, and the atherogenic coefficient were lower in individuals exposed to low temperatures for a longer time. In conclusion, human PBMC expresses the brown adipocytes marker CIDEA and the browning marker HOXC9, which, varying according to cold-exposure, possibly reflect changes in BAT activation and white fat browning.

scholarly journals Evaluation of Active Brown Adipose Tissue by the Use of Hyperpolarized [1-13C]Pyruvate MRI in Mice

2018 ◽  
Vol 19 (9) ◽  
pp. 2597 ◽  
Author(s):  
Mette Riis-Vestergaard ◽  
Peter Breining ◽  
Steen Pedersen ◽  
Christoffer Laustsen ◽  
Hans Stødkilde-Jørgensen ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Fdg Pet ◽  
Metabolic Diseases ◽  
Uncoupling Protein ◽  
Protein Levels ◽  
Positron Emission ◽  
Brown Adipose

The capacity to increase energy expenditure makes brown adipose tissue (BAT) a putative target for treatment of metabolic diseases such as obesity. Presently, investigation of BAT in vivo is mainly performed by fluoro-d-glucose positron emission tomography (FDG PET)/CT. However, non-radioactive methods that add information on, for example, substrate metabolism are warranted. Thus, the aim of this study was to evaluate the potential of hyperpolarized [1-13C]pyruvate Magnetic Resonance Imaging (HP-MRI) to determine BAT activity in mice following chronic cold exposure. Cold (6 °C) and thermo-neutral (30 °C) acclimated mice were scanned with HP-MRI for assessment of the interscapular BAT (iBAT) activity. Comparable mice were scanned with the conventional method FDG PET/MRI. Finally, iBAT was evaluated for gene expression and protein levels of the specific thermogenic marker, uncoupling protein 1 (UCP1). Cold exposure increased the thermogenic capacity 3–4 fold (p < 0.05) as measured by UCP1 gene and protein analysis. Furthermore, cold exposure as compared with thermo-neutrality increased iBAT pyruvate metabolism by 5.5-fold determined by HP-MRI which is in good agreement with the 5-fold increment in FDG uptake (p < 0.05) measured by FDG PET/MRI. iBAT activity is detectable in mice using HP-MRI in which potential changes in intracellular metabolism may add useful information to the conventional FDG PET studies. HP-MRI may also be a promising radiation-free tool for repetitive BAT studies in humans.

Phosphorylation of STAT3 in hypothalamic nuclei is stimulated by lower doses of leptin than are needed to inhibit food intake

2021 ◽  
Author(s):  
Ruth B.S. Harris
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Random Order ◽  
Progressive Increase ◽  
Female Rats ◽  
Male Rats ◽  
Sprague Dawley ◽  
Hypothalamic Nuclei ◽  
Brown Adipose ◽  
Integrated Response

This experiment investigated which hypothalamic nuclei were activated by a dose of leptin that inhibited food intake. Food intake, energy expenditure, respiratory exchange ratio (RER) and intrascapular brown adipose tissue (IBAT) temperature were measured in male and female Sprague Dawley rats for 36 hours following an intraperitoneal injection of 0, 50, 200, 500 or 1000 mg leptin/kg with each rat tested with each dose of leptin in random order. In both males and females RER and 12 hour food intake and were inhibited only by 1000 mg leptin/kg, but there was no effect on energy expenditure or IBAT temperature. At the end of the experiment pSTAT3 immunoreactivity was measured one hour after injection of 0, 50, 500 or 1000 mg leptin/kg. In male rats the lowest dose of leptin produced a maximal activation of STAT3 in the Arc and nucleus of the solitary tract (NTS). There was no response in the dorsomedial hypothalamus but there was a progressive increase in VMH pSTAT3 with increasing doses of leptin. In female rats there was no significant change in Arc pSTAT3, NTS activation was maximal with 500 mg leptin/kg, but only the highest dose of leptin increased VMH pSTAT3. These results suggest that the VMH plays an important role in the energetic response to elevations of circulating leptin, but do not exclude the possibility that multiple nuclei provide the appropriate integrated response to hyperleptinemia.

Progesterone does not alter sympathetic activity in tissues involved in energy balance

1996 ◽  
Vol 134 (4) ◽  
pp. 508-512
Author(s):  
Marisa Puerta ◽  
César Venero ◽  
Carmen Castro ◽  
María Abelenda
Keyword(s):  
Nervous System ◽  
Energy Balance ◽  
Food Intake ◽  
Sympathetic Nervous System ◽  
Sympathetic Activity ◽  
Female Rats ◽  
Noradrenaline Content ◽  
Brown Adipose ◽  
Energy Stores ◽  
Sympathetic Nervous

Puerta M, Venero C, Castro C, Abelenda M. Progesterone does not alter sympathetic activity in tissues involved in energy balance. Eur J Endocrinol 1996;134:508–12. ISSN 0804–4643 Female rats acclimated to thermoneutrality to avoid cold influences received progesterone by means of subcutaneous implants. They increased their food intake and body weight above the values recorded in control animals. None the less, despite the enhanced food intake, no sign of activation of the sympathetic nervous system was observed, as judged by the unaltered noradrenaline content, half-life and turnover rate in brown adipose tissue, pancreas and heart. This indicates that progesterone increases food intake but prevents non-energy-conservation processes regulated by the sympathetic nervous system from taking place. Thus, it facilitates in two different ways the building up of energy stores. Because overfeeding induced by palatable diets increases the sympathetic tone to the organs studied, it is suggested that the central mechanisms regulating energy balance are probably influenced in a different manner by progesterone than by the sensory properties of palatable diets. M Puerta, Departamento de Biología Animal II (Fisiología Animal), Facultad de Ciencias Biológicas, Universidad Complutense de Madrid, E-28040 Madrid, Spain

Sign in / Sign up

Export Citation Format

Share Document