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’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
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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
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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
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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
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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
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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
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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
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-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
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Institute of Experimental Medicine, Institut für Biochemie and Zellbiologie, Centre for Behavioral Brain Sciences, Hungarian Academy of Sciences, Szigony 43, 1083 Budapest, Hungary
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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
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Introduction Placental insufficiency restricts the transfer of oxygen and nutrients to the fetus, which leads to fetal hypoxemia, hypoglycemia, and intrauterine growth restriction (IUGR) ( Pardi et al. 1993 , Resnik 2002 ). Under hypoxemic
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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
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Abstract
The secretion of pancreatic polypeptide (PP) is regulated by fluctuations in blood glucose concentrations and food intake, in which vagal-cholinergic mechanisms play an important role, especially for the cephalic phase of PP secretion. In this study, we examined whether central cholinergic mechanisms are also important for PP secretion by relaying information in the brain to the vagus nerve and the muscarinic cholinergic receptors in the pancreas.
Atropine sulfate (20–200 μg) was administered into the lateral cerebral ventricle and its effects on the basal secretion of PP as well as the secretions stimulated by insulin-induced hypoglycemia (Actrapid MC, 0·25 U/kg) and a mixed meal (243 kcal) were studied in seven dogs. Intralateral cerebroventricular (ILV) atropine (100 and 200 μg) abolished the fluctuations in basal PP secretion without appearing in the plasma. Pretreatment with 20, 100, and 200 μg ILV atropine significantly decreased the PP response to insulin-induced hypoglycemia, with the integrated PP response to 58, 32, and 26% of that of controls respectively. Atropine (100 μg ILV) significantly reduced the postprandial PP secretion in both the cephalic and the gastrointestinal phases, whereas increased insulin and glucose levels were unaffected.
Centrally administered atropine was able to suppress the basal secretion of PP as well as the secretions stimulated by hypoglycemia and food intake. These findings suggest that (1) the spontaneous release of PP is governed by an oscillating, central cholinergic tone, and (2) the stimulating PP secretion is, at least in part, regulated by the central cholinergic system.
Journal of Endocrinology (1997) 154, 311–317
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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.
