Search Results
Search for other papers by Jasleen Kaur in
Google Scholar
PubMed
Search for other papers by Elizabeth R Seaquist in
Google Scholar
PubMed
’Alessio 2015 ) ( Fig. 1 ). For almost 50 years, glucagon has been understood to be a hyperglycemic factor that opposes the effects of insulin and has been used pharmacologically to correct insulin-induced hypoglycemia. More recently, research has increased our
Search for other papers by Mariana Rosolen Tavares in
Google Scholar
PubMed
Search for other papers by Renata Frazao in
Google Scholar
PubMed
Search for other papers by Jose Donato Jr in
Google Scholar
PubMed
particularly evident in situations of metabolic stress, such as hypoglycemia ( Roth et al. 1963 ), prolonged food deprivation ( Zhao et al. 2010 ), physical exercise ( Veldhuis et al. 2015 ), and even pregnancy ( Gatford et al. 2017 ), which is a
Search for other papers by Lei Huang in
Google Scholar
PubMed
Search for other papers by Bin Qiu in
Google Scholar
PubMed
Search for other papers by Lin Yuan in
Google Scholar
PubMed
Search for other papers by Lili Zheng in
Google Scholar
PubMed
Search for other papers by Qiang Li in
Google Scholar
PubMed
Search for other papers by Shigong Zhu in
Google Scholar
PubMed
relationship between ghrelin in the DVC and energy conditions, such as fasting, hyperglycemia, and hypoglycemia. It has been reported that the vagus nerve is an essential pathway that transmits peripheral ghrelin information to the brain stem ( Berthoud
Department of Clinical Research, Cardiovascular Research Institute, Institute of Medical Biology, Department of Surgery, Singapore General Hospital, Block A, #03-04, 7 Hospital Drive, SingHealth Research Facility, Singapore, 169611 Singapore
Search for other papers by Shiying Shao in
Google Scholar
PubMed
Search for other papers by Yun Gao in
Google Scholar
PubMed
Department of Clinical Research, Cardiovascular Research Institute, Institute of Medical Biology, Department of Surgery, Singapore General Hospital, Block A, #03-04, 7 Hospital Drive, SingHealth Research Facility, Singapore, 169611 Singapore
Search for other papers by Bing Xie in
Google Scholar
PubMed
Search for other papers by Fei Xie in
Google Scholar
PubMed
Department of Clinical Research, Cardiovascular Research Institute, Institute of Medical Biology, Department of Surgery, Singapore General Hospital, Block A, #03-04, 7 Hospital Drive, SingHealth Research Facility, Singapore, 169611 Singapore
Search for other papers by Sai Kiang Lim in
Google Scholar
PubMed
Department of Clinical Research, Cardiovascular Research Institute, Institute of Medical Biology, Department of Surgery, Singapore General Hospital, Block A, #03-04, 7 Hospital Drive, SingHealth Research Facility, Singapore, 169611 Singapore
Search for other papers by GuoDong Li in
Google Scholar
PubMed
encapsulated cells resulted in a high frequency of severe hypoglycemia with 60% of mice dying within 40 days. On the other hand, it took a long time to correct hyperglycemia when 1 million encapsulated cells were transplanted. Blood glucose and body weight were
Search for other papers by L A Santiago in
Google Scholar
PubMed
Search for other papers by D A Santiago in
Google Scholar
PubMed
Search for other papers by L C Faustino in
Google Scholar
PubMed
Search for other papers by A Cordeiro in
Google Scholar
PubMed
Search for other papers by P C Lisboa in
Google Scholar
PubMed
Search for other papers by F E Wondisford in
Google Scholar
PubMed
Search for other papers by C C Pazos-Moura in
Google Scholar
PubMed
Search for other papers by T M Ortiga-Carvalho in
Google Scholar
PubMed
-old, n =5–7. AUC, area under the curve. * TRβ WT/WT and TRβ WT/Δ337T versus TRβ Δ337T/Δ337T , P <0.05, # TRβ WT/WT and TRβ WT/Δ337T versus TRβ Δ337T/Δ337T , P <0.01. At time points 60, 90 and 120 min, mice presenting severe hypoglycemia were
Search for other papers by Anna Fodor in
Google Scholar
PubMed
Search for other papers by Ottó Pintér in
Google Scholar
PubMed
Search for other papers by Ágnes Domokos in
Google Scholar
PubMed
Search for other papers by Kristina Langnaese in
Google Scholar
PubMed
Search for other papers by István Barna in
Google Scholar
PubMed
Institute of Experimental Medicine, Institut für Biochemie and Zellbiologie, Centre for Behavioral Brain Sciences, Hungarian Academy of Sciences, Szigony 43, 1083 Budapest, Hungary
Search for other papers by Mario Engelmann in
Google Scholar
PubMed
Search for other papers by Dóra Zelena in
Google Scholar
PubMed
immediately before (at 0 min) and 15, 30, 60, 90, and 120 min after injection. Insulin injection After 18 h of fasting, hypoglycemia was induced by i.p. injection of Actrapid (rapid insulin, 3NE/2 ml/kg; Novo Nordisk, Bagsvaerd, Denmark). One hour later, the
Search for other papers by J D Bailey in
Google Scholar
PubMed
Search for other papers by J G Berardinelli in
Google Scholar
PubMed
Search for other papers by T E Rocke in
Google Scholar
PubMed
Search for other papers by R A Bessen in
Google Scholar
PubMed
preclinical obesity and hyperinsulinemia. However, Carp et al . (1990) further reported that by 18 weeks p.i., fasted 139H scrapie-infected hamsters developed hypoglycemia. This conclusion was based upon a single glucose evaluation at 2 h post
Search for other papers by CD McMahon in
Google Scholar
PubMed
Search for other papers by TH Elsasser in
Google Scholar
PubMed
Search for other papers by DR Gunter in
Google Scholar
PubMed
Search for other papers by LG Sanders in
Google Scholar
PubMed
Search for other papers by BP Steele in
Google Scholar
PubMed
Search for other papers by JL Sartin in
Google Scholar
PubMed
High doses of lipopolysaccharide (LPS) induce transient hyperglycemia, then chronic hypoglycemia and increased insulin resistance. In addition, appetite is reduced, while body temperature and concentrations of cortisol and tumor necrosis factor alpha (TNFalpha) are elevated. Furthermore, concentrations of GH and IGF-I are reduced in cattle. The objectives of this study were to determine whether a gonadal steroid implant (20 mg estrogen and 200 mg progesterone) given to endotoxemic steers would: (1) reduce hyperglycemia, reduce hypoglycemia, reduce insulin resistance, (2) reduce changes in concentrations of GH and IGF-I, (3) reduce inappetence and reduce concentrations of blood urea nitrogen (BUN) and non-esterified fatty acids (NEFA), and (4) reduce fever and concentrations of TNFalpha and cortisol. Holstein steers were assigned within a 2x2 factorial arrangement of treatments as follows (n=5 per group): C/C, no steroid and vehicle; S/C, steroid and vehicle; C/E, no steroid and LPS (1 microg/kg body weight (BW), i.v.); S/E, steroid and endotoxin. Steroid implants were given at 20 weeks of age (day 0) and serial blood samples (15 min) were collected on day 14 for 8 h, with vehicle or LPS injected after 2 h. Intravenous glucose tolerance tests (100 mg/kg BW) were carried out at 6 h and 24 h. Hyperglycemia was 67% lower (P<0.05) in S/E- compared with C/E-treated steers between 30 and 150 min after i.v. injection of LPS. Hypoglycemia developed after 4 h and insulin resistance was greater in S/E- compared with C/E-treated steers (P<0. 05) at 6 and 24 h. Concentrations of IGF-I were restored earlier in steroid-treated steers than in controls. Concentrations of GH were not affected by steroids, but increased 1 h after injection of LPS, then were reduced for 2 h. Appetite was greater (P<0.05) in S/E- (2.1% BW) compared with C/E-treated steers (1.1% BW) (pooled s.e.m.=0.3). Concentrations of NEFA increased after injecting LPS, but concentrations were lower (P<0.05) in S/E- compared with C/E-treated steers. LPS did not affect concentrations of BUN, but concentrations were lower in steroid-treated steers. Steroids did not affect body temperature or concentrations of TNFalpha and cortisol. In summary, gonadal steroids reduce hyperglycemia, reduce inappetence and tissue wasting, but increase insulin resistance. Furthermore, concentrations of IGF-I are restored earlier in steroid-treated than in non-steroid-treated steers injected with LPS. It is concluded that gonadal steroids reduce severity of some endocrine and metabolic parameters associated with endotoxemia. However, it is unlikely that gonadal steroids acted via anti-inflammatory and immunosuppressive actions of glucocorticoids or through reducing concentrations of cytokines.
Search for other papers by A P Santos-Silva in
Google Scholar
PubMed
Search for other papers by E Oliveira in
Google Scholar
PubMed
Search for other papers by C R Pinheiro in
Google Scholar
PubMed
Search for other papers by A L Nunes-Freitas in
Google Scholar
PubMed
Search for other papers by Y Abreu-Villaça in
Google Scholar
PubMed
Search for other papers by A C Santana in
Google Scholar
PubMed
Search for other papers by C C Nascimento-Saba in
Google Scholar
PubMed
Search for other papers by J F Nogueira-Neto in
Google Scholar
PubMed
Search for other papers by A M Reis in
Google Scholar
PubMed
Search for other papers by E G Moura in
Google Scholar
PubMed
Search for other papers by P C Lisboa in
Google Scholar
PubMed
Exposure to tobacco smoke is related to changes in energy balance regulation and several endocrine dysfunctions. Previously, we showed that maternal nicotine (the main addictive compound of tobacco) exposure exclusively during lactation affects biochemical profiles in mothers, milk, and pups. As the possible consequences for mothers and offspring of maternal smoking during lactation are still unknown, we evaluated the effects of tobacco smoke exposure on nutritional, biochemical, and hormonal parameters in dams and pups at weaning. After 72 h from birth, lactating rats were divided into two groups: smoke-exposed (S) in a cigarette-smoking machine, 4×1 h per day throughout the lactation period without pups; control (C), rats were treated the same as the experimental group but exposed to filtered air. Dams and pups were killed at weaning (21 days of lactation). Body weight and food intake were evaluated. Milk, blood, visceral fat, adrenal, and carcass were collected. S dams showed hyperprolactinemia (+50%), hypoinsulinemia (−40%), hypoleptinemia (−46%), as well as lower triglycerides (−53%) and very low-density lipoprotein cholesterol (−50%). Milk of S dams had higher lactose (+52%) and triglycerides (+78%). S pups presented higher body protein (+17%), lower total (−24%) and subcutaneous fat contents (−25%), hypoglycemia (−11%), hyperinsulinemia (+28%), hypocorticosteronemia (−40%), lower adrenal catecholamine content (−40%), hypertriglyceridemia (+34%), higher high-density lipoprotein cholesterol (+16%), and lower low-density lipoprotein cholesterol (−45%). In conclusion, tobacco smoke exposure leads to changes in nutritional, biochemical, and hormonal parameters in dams and, passively through the milk, may promote several important metabolic disorders in the progeny.
Search for other papers by MR Pickard in
Google Scholar
PubMed
Search for other papers by AJ Leonard in
Google Scholar
PubMed
Search for other papers by LM Ogilvie in
Google Scholar
PubMed
Search for other papers by PR Edwards in
Google Scholar
PubMed
Search for other papers by IM Evans in
Google Scholar
PubMed
Search for other papers by AK Sinha in
Google Scholar
PubMed
Search for other papers by RP Ekins in
Google Scholar
PubMed
Maternal hypothyroidism impairs fetal growth in the rat, but the mechanisms by which this occurs are unknown. Since the fetus derives its glucose supply from the mother, and maternal thyroidectomy may disturb maternal and placental glucose metabolism, we postulated that maternal and/or placental glucose metabolic compromise may contribute to fetal growth retardation in hypothyroid dams. Feto-placental growth, tissue glycogen stores and glucose levels in sera and amniotic fluid were determined in rat dams partially thyroidectomized (TX) before pregnancy and in euthyroid controls. Fetal body weight at 16, 19 and 21 days gestation (d.g.) was related to pre-mating maternal serum total thyroxine (TT(4)) levels; permanent fetal growth retardation occurred in severely (TX(s); pre-mating maternal serum TT(4) 16.19 nM) - but not in moderately (TX(m)) - hypothyroid dams. In TX(s) dams, glycogen concentration was elevated in maternal liver and in the fetal side of the placenta at 16 and 19 d.g., and in the maternal side of the placenta at 19 and 21 d.g., despite maternal euglycemia. In contrast, fetal liver glycogen concentration was deficient in TX(m) dams at 19 d.g. and in TX(s) dams at 19 and 21 d.g., and fetal hypoglycemia occurred in TX(s) dams at 21 d.g. Multiple regression analyses indicate that these fetal deficits are strongly associated with the retardation in fetal growth, while the elevated maternal liver and placental glycogen concentrations have no impact on fetal growth near term. The mechanisms by which severe maternal hypothyroidism permanently retards rat fetal growth remain to be determined.
