Hypothyroidism Alters the Uterine Lipid Levels in Pregnant Rabbits and Affects the Fetal Size

Background: Hypothyroidism has been related to low-weight births, abortion and prematurity, which have been associated with changes in the content of glycogen and vascularization of the placenta. Since hypothyroidism can cause dyslipidemia, it may affect the lipid content in the uterus affecting the development of fetuses. Objective: To investigate the effect of hypothyroidism on the lipid levels in serum and uterus during pregnancy and their possible association with the size of fetuses. Methods: Adult female rabbits were grouped in control (n = 6) and hypothyroid (n = 6; treated with methimazole for 29 days before and 19 days after copulation). Food intake and body weight were daily registered. At gestational day 19 (GD19), dams were sacrificed under an overdose of anesthesia. Morphometric measures of fetuses were taken. Total cholesterol (TC), triglyceride (TAG), and glucose concentrations were quantified in blood, uterus and ovaries of dams. The expression of uterine 3β- hydroxysteroid dehydrogenase (3β-HSD) was quantified by Western blot. Results: Hypothyroidism reduced food intake and body weight of dams, as well as promoted low abdominal diameters of fetuses. It did not induce dyslipidemia and hyperglycemia at GD19 and did not modify the content of lipids in the ovary. However, it reduced the content of TAG and TC in the uterus, which was associated with uterine hyperplasia and an increased expression of 3β-HSD in the uterus. Conclusion: Hypothyroidism alters the lipid content in the uterus that might subsequently affect the energy production and lipid signaling important to fetal development.

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Effects of hormones and hypoglycemic agents on testicular fat in the rat

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1961.200.6.1277 ◽

1961 ◽

Vol 200 (6) ◽

pp. 1277-1284 ◽

Cited By ~ 69

Author(s):

T. C. Smith ◽

L. Will ◽

J. Oleson ◽

K. -F. Benitz ◽

J. Perrine ◽

...

Keyword(s):

Growth Hormone ◽

Body Weight ◽

Blood Glucose ◽

Food Intake ◽

Lipid Content ◽

Fat Body ◽

Hypoglycemic Agents ◽

Hydrocortisone Acetate ◽

Simultaneous Measurements ◽

Fat Bodies

Response of transplanted and nontransplanted fat bodies to various hormones, tolbutamide, and hypoglycin A was compared by measuring the amount of lipids in the dissected fat bodies after 2 weeks treatment. Simultaneous measurements of food intake and body weight were made to serve as a basis for evaluating the effects on fat. Protamine zinc insulin produced an increase in lipid content of the testicular fat body, accompanied by elevation in food intake in three of five experiments; hydrocortisone acetate, triamcinolone or its 16,21-diacetate, or diethylstilbestrol brought about decreases in lipid with either no change or a decline in food intake; epinephrine·HCl or growth hormone elicited decreases in lipid without significantly influencing food intake or body weight. Generally, transplanted fat was more responsive to these agents than the undisturbed fat body. Both tolbutamide and hypoglycin A decreased lipids in the transplant without affecting those in untransplanted fat. Food intake, body weight, and blood glucose were not changed.

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11β-Hydroxysteroid Dehydrogenase Type 1 (11β-HSD1) Inhibitors Still Improve Metabolic Phenotype in Male 11β-HSD1 Knockout Mice Suggesting Off-Target Mechanisms

Endocrinology ◽

10.1210/en.2013-1613 ◽

2013 ◽

Vol 154 (12) ◽

pp. 4580-4593 ◽

Cited By ~ 19

Author(s):

Erika Harno ◽

Elizabeth C. Cottrell ◽

Alice Yu ◽

Joanne DeSchoolmeester ◽

Pablo Morentin Gutierrez ◽

...

Keyword(s):

Body Weight ◽

Food Intake ◽

Knockout Mice ◽

Hydroxysteroid Dehydrogenase ◽

Metabolic Parameters ◽

Metabolic Effects ◽

Metabolic Phenotype ◽

Positive Effects ◽

Compound C

The enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) is a target for novel type 2 diabetes and obesity therapies based on the premise that lowering of tissue glucocorticoids will have positive effects on body weight, glycemic control, and insulin sensitivity. An 11β-HSD1 inhibitor (compound C) inhibited liver 11β-HSD1 by >90% but led to only small improvements in metabolic parameters in high-fat diet (HFD)–fed male C57BL/6J mice. A 4-fold higher concentration produced similar enzyme inhibition but, in addition, reduced body weight (17%), food intake (28%), and glucose (22%). We hypothesized that at the higher doses compound C might be accessing the brain. However, when we developed male brain-specific 11β-HSD1 knockout mice and fed them the HFD, they had body weight and fat pad mass and glucose and insulin responses similar to those of HFD-fed Nestin-Cre controls. We then found that administration of compound C to male global 11β-HSD1 knockout mice elicited improvements in metabolic parameters, suggesting “off-target” mechanisms. Based on the patent literature, we synthesized another 11β-HSD1 inhibitor (MK-0916) from a different chemical series and showed that it too had similar off-target body weight and food intake effects at high doses. In summary, a significant component of the beneficial metabolic effects of these 11β-HSD1 inhibitors occurs via 11β-HSD1–independent pathways, and only limited efficacy is achievable from selective 11β-HSD1 inhibition. These data challenge the concept that inhibition of 11β-HSD1 is likely to produce a “step-change” treatment for diabetes and/or obesity.

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A novel traditional Chinese medicine ameliorates fatigue-induced cardiac hypertrophy and dysfunction via regulation of energy metabolism

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00731.2018 ◽

2019 ◽

Vol 316 (6) ◽

pp. H1378-H1388 ◽

Cited By ~ 1

Author(s):

Rong Huang ◽

Yuan-Chen Cui ◽

Xiao-Hong Wei ◽

Chun-Shui Pan ◽

Quan Li ◽

...

Keyword(s):

Body Weight ◽

Energy Metabolism ◽

Chinese Medicine ◽

Food Intake ◽

Traditional Chinese Medicine ◽

Cardiac Hypertrophy ◽

Western Blot ◽

Prolonged Exercise ◽

Heart Function ◽

Heart Weight

Prolonged exercise and exercise training can adversely affect cardiac function in some individuals. QiShenYiQi Pills (QSYQ), which are a compound Chinese medicine, have been previously shown to improve pressure overload-induced cardiac hypertrophy. We hypothesized that QSYQ can ameliorate as well the fatigue-induced cardiac hypertrophy. This study was to test this hypothesis and underlying mechanism with a focus on its role in energy regulation. Male Sprague-Dawley rats were used to establish exercise adaptation and fatigue model on a motorized rodent treadmill. Echocardiographic analysis and heart function test were performed to assess heart systolic function. Food-intake weight/body weight and heart weight/body weight were assessed, and hematoxylin and eosin staining and immunofluorescence staining of myocardium sections were performed. ATP synthase expression and activity and ATP, ADP, and AMP levels were assessed using Western blot and ELISA. Expression of proteins related to energy metabolism and IGF-1R signaling was determined using Western blot. QSYQ attenuated the food-intake weight/body weight decrease, improved myocardial structure and heart function, and restored the expression and distribution of myocardial connexin 43 after fatigue, concomitant with an increased ATP production and a restoration of metabolism-related protein expression. QSYQ upgraded the expression of IGF-1R, P-AMPK/AMPK, peroxisome proliferator-activated receptor-γ coactivator-1α, nuclear respiratory factor-1, P-phosphatidylinositol 3-kinase (PI3K)/PI3K, and P-Akt/Akt thereby attenuated the dysregulation of IGF-1R signaling after fatigue. QSYQ relieved fatigue-induced cardiac hypertrophy and enhanced heart function, which is correlated with its potential to improve energy metabolism by regulating IGF-1R signaling. NEW & NOTEWORTHY Prolonged exercise may impact some people leading to pathological cardiac hypertrophy. This study using an animal model of fatigue-induced cardiac hypertrophy provides evidence showing the potential of QiShenYiQi Pills, a novel traditional Chinese medicine, to prevent the cardiac adaptive hypertrophy from development to pathological hypertrophy and demonstrates that this effect is correlated with its capacity for regulating energy metabolism through interacting with insulin-like growth factor-1 receptor.

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The protective effect of nicotinamide riboside against age-induced hepatic disease in mice

10.7287/peerj.preprints.27705 ◽

2019 ◽

Author(s):

Xue Han ◽

Xiaogang Bao ◽

Qi Lou ◽

Xian Xie ◽

Shasang Zhou ◽

...

Keyword(s):

Body Weight ◽

Food Intake ◽

Lipid Content ◽

Mice Model ◽

Alcoholic Fatty Liver ◽

Nicotinamide Riboside ◽

Aged Mice ◽

Beneficial Effects ◽

Biochemical Assays ◽

Normal Chow

Background & Aims. Aging is one of the key triggers of non-alcoholic fatty liver disease (NAFLD). Yet, the pathomechanism of the age-associated NAFLD is not fully understood. Nicotinamide adenine dinucleotide (NAD), an ubiquitous coenzyme, has beneficial effects on aging. Here, we investigated the actions of NAD precursors nicotinamide riboside (NR) on the development of age-induced NAFLD. Methods. NR supplied food (2.5g/kg food) was applied to aged mice for three months. Changes of body weight, food intake, hepar weight and fat pat mass were measured. The serum concentrations of lipid content, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and NAD were determined by biochemical assays. Pathological assessment and immunohistochemistry analysis of hepatic tissues were used to evaluate the effect of NR on NAFLD development and inflammation infiltrated. Results. NR significantly reduced fat pat mass, lipid content and AST in aged mice, but didn't modify in terms of body weight, food intake, hepar weight and ALT in aged mice. Given normal chow, aged mice displayed decline of NAD concentration. In aged mice model, moderate NAFLD phenotypes, including steatosis and hepatic fibrosis (Masson's trichrome staining and TGF-β staining) were observed in liver. In addition, Kupffer cells accumulated and pro-inflammatory cytokines expression were more aggravated in hepatic tissues. Whereas, NR administration completely corrected these NAFLD phenotypes and inflammation infiltrated in liver. Conclusion. NR has benefits on age-associated lipid accumulation and hepatic steatosis, and the oral uptake of NR may be a promising strategy to prevent the progression of NAFLD.

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Recombinant leptin exchanges between parabiosed mice but does not reach equilibrium

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1997.272.6.r1800 ◽

1997 ◽

Vol 272 (6) ◽

pp. R1800-R1808 ◽

Cited By ~ 8

Author(s):

R. B. Harris ◽

J. Zhou ◽

D. S. Weigle ◽

J. L. Kuijper

Keyword(s):

Body Weight ◽

Food Intake ◽

Body Temperature ◽

Western Blot ◽

Blot Analysis ◽

Half Life ◽

Serum Insulin ◽

Liver Weight ◽

Gut Content ◽

Serum Leptin

Parabiosis experiments suggest that ob/ob mice are deficient in a circulating "lipostatic" signal but respond to such a signal when it is delivered in the cross circulation from their parabiotic partner. Identification of leptin as the mutation in ob/ob mice leads to the assumption that leptin is the lipostatic signal. The objective of these experiments was to determine the circulating half-life of leptin and to demonstrate whether it exchanged between parabiosed mice. Measurement of disappearance of recombinant leptin from serum in SWRJ mice indicated a circulating half-life of approximately 36 min. Single ob/ob mice or one member of a parabiosed pair of ob/ob mice received 50 micrograms recombinant murine leptin in two intraperitoneal injections a day for 10 days, starting 40 days after parabiosis surgery. Control mice and pairs received equivalent injections of vehicle. In single mice, leptin significantly reduced food intake, body weight, serum insulin, and pancreatic and liver weight. Leptin treatment of one member of a parabiosed pair of ob/ob mice reduced serum insulin, gut content (an index of food intake), and body fat in both partners. The injected parabiont lost more fat than its partner, and body temperature was increased only in the injected mouse, indicating that leptin did not reach equilibrium in the two animals. This was confirmed by Western blot analysis of serum leptin measured 2 h after injection. Therefore, although leptin can exchange between parabionts, its half-life is inadequate to allow equilibrium when a large concentration gradient exists between partners.

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Influence of Thyroid Status on Body Weight Gain, Food Intake and Serum Lipid Levels in Genetically Obese Zucker Rats

Journal of Nutrition ◽

10.1093/jn/117.1.159 ◽

1987 ◽

Vol 117 (1) ◽

pp. 159-163 ◽

Cited By ~ 2

Author(s):

Annie Loireau ◽

Paul Dumas ◽

Nicole Autissier ◽

Raymond Michel

Keyword(s):

Body Weight ◽

Weight Gain ◽

Food Intake ◽

Serum Lipid ◽

Body Weight Gain ◽

Zucker Rats ◽

Lipid Levels ◽

Thyroid Status ◽

Serum Lipid Levels ◽

Obese Zucker Rats

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The protective effect of nicotinamide riboside against age-induced hepatic disease in mice

10.7287/peerj.preprints.27705v1 ◽

2019 ◽

Author(s):

Xue Han ◽

Xiaogang Bao ◽

Qi Lou ◽

Xian Xie ◽

Shasang Zhou ◽

...

Keyword(s):

Body Weight ◽

Food Intake ◽

Lipid Content ◽

Mice Model ◽

Alcoholic Fatty Liver ◽

Nicotinamide Riboside ◽

Aged Mice ◽

Beneficial Effects ◽

Biochemical Assays ◽

Normal Chow

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Effect of different dietary lipid levels on growth performance, slaughter yield, chemical composition, and histology of liver and intestine of pikeperch, Sander lucioperca

Czech Journal of Animal Science ◽

10.17221/1298-cjas ◽

2011 ◽

Vol 56 (No. 3) ◽

pp. 136-149 ◽

Cited By ~ 10

Author(s):

A. Kowalska ◽

Z. Zakęś ◽

B. Jankowska ◽

K. Demska-Zakęś

Keyword(s):

Fatty Acids ◽

Body Weight ◽

Chemical Composition ◽

Polyunsaturated Fatty Acids ◽

Growth Performance ◽

Lipid Content ◽

Whole Body ◽

Lipid Levels ◽

Sander Lucioperca ◽

The Impact

In this study, 16-month-old pikeperch, Sander lucioperca, (initial body weight 280 g) were fed three diets with different lipid levels with the aim of determining the impact on the growth performance, hepatic and intestinal histological structure, chemical composition, and slaughter yield of this species. The fish were fed isoproteinaceous feeds (450 g protein/kg feed) containing 60 g lipids/kg feed (group F6), 100 g lipids/kg feed (group F10) and 180 g lipids/kg feed (group F18). No significant differences were noted among the treatment groups in body weight gain and in the feeding coefficients of experimental feeds (P > 0. 05). In the group of fish administered the diet with the lowest lipid content (group F6), the share of skinned fillet in the whole body weight was the highest (48% vs. 43% in group F18) (P < 0.05). No significant differences among groups were confirmed in the relative values of the viscera weight (4.8–5.8%) (P > 0.05). The highest values of the size of hepatocytes and their nuclei, intestinal cells, supranuclear vacuoles of enterocytes, and the degree of vacuolization in hepatocytes were determined in group F18 (P < 0.05), indicating histopathological changes. The highest body and viscera lipid contents were noted in individuals from group F18 (P < 0.05). The high lipid content in the viscera of fish from this group was linked to the significantly lowest content of protein and ash. The levels of lipids, protein, and ash were similar (P > 0.05) in the pikeperch fillets from the three feeding treatments. The levels of n-6 polyunsaturated fatty acids (n-6 PUFA) in the whole fish body, in the viscera and fillets (P < 0.05) were the significantly highest in group F18. Significant differences in n-3 polyunsaturated fatty acids (n-3 PUFA) among the groups were confirmed in the whole fish body and viscera (P < 0.05), while the values in the fillets were similar (P > 0.05). The n–3/n–6 index for the fish fillets ranged from 2.4 (group F18) to 4.7 (group F6) (P < 0.05). The levels of n-3 highly unsaturated fatty acids (n-3 HUFA), arachidonic acid (ARA) and docosahexaenoic acid (DHA) in the fillets of fish from the three dietary treatments were similar (P > 0.05). The fillets of fish from group F6, however, had the lowest levels of linolenic and linoleic acid (ALA and LA) and the highest levels of eicosapentaenoic acid (EPA) (P < 0.05).

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