Radiochemical assay of long-chain fatty acids using 63Ni as tracer

Ho, Ren-Jye

doi:10.1016/0003-2697(70)90337-4

Cited by 391 publications

(126 citation statements)

References 8 publications

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“…Lactate, glycerol, alanine, and ␤-hydroxybutyrate were measured in deproteinized whole blood using the method of Lloyd et al (24). Nonesterified fatty acids (NEFAs) were measured using the WAKO kit adopted for use on a centrifugal analyzer (25). A1C was determined in whole blood using the Variant II A1C cation-exchange HPLC kit system (26).…”

Section: Methodsmentioning

confidence: 99%

Effects of a Selective Serotonin Reuptake Inhibitor, Fluoxetine, on Counterregulatory Responses to Hypoglycemia in Healthy Individuals

et al. 2008

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OBJECTIVE-Hypoglycemia commonly occurs in intensivelytreated diabetic patients. Repeated hypoglycemia blunts counterregulatory responses, thereby increasing the risk for further hypoglycemic events. Currently, physiologic approaches to augment counterregulatory responses to hypoglycemia have not been established. Therefore, the specific aim of this study was to test the hypothesis that 6 weeks' administration of the selective serotonin reuptake inhibitor (SSRI) fluoxetine would amplify autonomic nervous system (ANS) and neuroendocrine counterregulatory mechanisms during hypoglycemia. RESEARCH DESIGN AND METHODS-A total of 20 healthy (10 male and 10 female) subjects participated in an initial single-step hyperinsulinemic (9 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 )-hypoglycemic (means Ϯ SE 2.9 Ϯ 0.1 mmol/l) clamp study and were then randomized to receive 6 weeks' administration of fluoxetine (n ϭ 14) or identical placebo (n ϭ 6) in a double-blind fashion. After 6 weeks, subjects returned for a second hypoglycemic clamp. Glucose kinetics were determined by three-tritiated glucose, and muscle sympathetic nerve activity (MSNA) was measured by microneurography.RESULTS-Despite identical hypoglycemia (2.9 Ϯ 0.1 mmol/l) and insulinemia during all clamp studies, key ANS (epinephrine, norepinephrine, and MSNA but not symptoms), neuroendocrine (cortisol), and metabolic (endogenous glucose production, glycogenolysis, and lipolysis) responses were increased (P Ͻ 0.01) following fluoxetine.CONCLUSIONS-This study demonstrated that 6 weeks' administration of the SSRI fluoxetine can amplify a wide spectrum of ANS and metabolic counterregulatory responses during hypoglycemia in healthy individuals. These data further suggest that serotonergic transmission may be an important mechanism in modulating sympathetic nervous system drive during hypoglycemia in healthy individuals. Diabetes 57:2453-2460, 2008 S everal reports have indicated that fluoxetine could have metabolic effects and influence carbohydrate metabolism (1-3). In fact, there have been three case studies reporting the occurrence of hypoglycemia related to the use of selective serotonin reuptake inhibitors (SSRIs) in depressed patients with and without diabetes (4 -6). However, although SSRIs are potent inhibitors of neuronal serotonin uptake, they also have the ability to block norepinephrine transport (7). This could increase sympathetic outflow activity (2,8). Baudrie and Chaouloff (9) have previously reported an increased hyperglycemic response to 2-deoxy-D-glycose in conscious rats following serotononergic receptor antagonists, implying increased counterregulation in these animals.A subsequent study by Perry and Fuller (2) demonstrated that systemic injection of the SSRI fluoxetine in rats resulted in threefold increases of hypothalamic norepinephrine release, thereby providing a mechanistic basis for SSRIs to modulate sympathetic nervous system activity. A later study by Bymaster et al. (3) examined the specificity of five different SSRIs (fluoxetine, citalopram, fluvoxamine, paroxe...

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Section: Methodsmentioning

confidence: 99%

Effects of a Selective Serotonin Reuptake Inhibitor, Fluoxetine, on Counterregulatory Responses to Hypoglycemia in Healthy Individuals

et al. 2008

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“…Lactate, glycerol, alanine, and -h y d r o x y b u t y r a t e were measured in deproteinized whole blood using the method of Lloyd et al (23). N o n e s t e r i fied fatty acids (NEFAs) were measured using the Wako kit (Wako, Richmond, VA) adopted for use on a centrifugal analyzer (24).…”

Section: Experimental Designmentioning

confidence: 99%

Hypoglycemic counterregulatory responses differ between men and women with type 1 diabetes.

2000

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The aim of this study was to determine whether s e x-related differences occur in counterregulatory responses to hypoglycemia in adult type 1 diabetic patients. Experiments were carried out on 16 (8 men/8 women) type 1 diabetic patients and compared with 16 (8 men/8 women) age-and weight-matched normal individuals. Men and women with type 1 diabetes were matched for age (26 ± 2 vs. 25 ± 1 years), duration of diabetes (9 ± 1 vs. 8 ± 1 years), glycemic control (HbA 1 c 7.7 ± 0.3 vs. 7.8 ± 0.2%), and weight (BMI 22.8 ± 1 vs. 22.1 ± 1 k g / m 2 ), respectively. After normalizing plasma glucose overnight, patients underwent a 2-h hyperinsulinemic-hypoglycemic clamp study. Plasma glucose (3.0 ± 0.1 mmol/l) and insulin (510 ± 48 pmol/l) levels were equated in all groups. Plasma epinephrine, norepinephrine, growth hormone (GH), muscle sympathetic nerve activity (MSNA), and endogenous glucose production (EGP) responses were significantly lower (P < 0.01) in type 1 diabetic women compared with men. Autonomic symptom scores, lipid oxidation, none s t e r i fied fatty acids (NEFAs), and glycerol responses were equivalent between men and women with type 1 diabetes despite significantly reduced sympathoadrenal and MSNA responses in women. Autonomic n e r v o u s system (ANS) and EGP responses were equivalent in t y p e 1 diabetic and normal individuals. However, lipid oxidation (assessed by indirect calorimetry), glycerol, and NEFA responses were increased (P < 0.01) in t y p e 1 diabetic patients compared with normal control subjects. We conclude that counterregulatory responses to fixed hypoglycemia differ markedly in men and women with type 1 diabetes: 1 ) sympathetic n e r v o u s system, GH, and EGP responses are significantly reduced in type 1 diabetic women, 2) autonomic symptom awareness and lipolytic responses appear to be relatively increased in type 1 diabetic women compared with men, and 3) during conditions of similar hyperinsulinemic hypoglycemia and ANS drive, lipid oxidation and lipolytic responses can be increased in type 1 diabetic patients compared with normal individuals. Diabetes 4 9 :6 5-72, 2000 R ecent studies have demonstrated that a wide spectrum of neuroendocrine counterregulatory responses to hypoglycemia are reduced in healthy young women (1-4). Included in this array of altered responses are the key counterregulatory hormones glucagon and epinephrine (EPI). These findings tend to explain why plasma glucose levels fall to a lower level during fasting in women (5). If a similar spectrum of reduced neuroendocrine counterregulatory responses exist in women with type 1 diabetes, then an increased incidence of hypoglycemia might be expected in these individuals. However, data from the Diabetes Control and Complications Trial demonstrate that the frequency of hypoglycemia is sex neutral in t y p e 1 diabetes (6). This finding appears somewhat incongruous with data on normal women and poses the question whether counterregulatory responses to hypoglycemia are similar in healthy and type 1 diabetic women. ...

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“…They were analysed immediately or stored at -2 0 ~ Fat content was determined as fatty acids [23] after saponification of the whole muscle, assuming a mean molecular weight of 281. DNA was determined by the method of Burton [24] with calf thymus DNA as standard.…”

Section: Estimation Of Dna and Fat Content Of Musclesmentioning

confidence: 99%

A histochemical and morphological study of skeletal muscle from obese hyperglycaemic ob/ob mice

almond

Enser

1984

Diabetologia

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Summary. The histochemical and morphological charactefis= tics of muscles from lean and obese hyperglycaemic ob/ob mice were compared to determine the nature of the low skeletal muscle mass of the latter: Gastrocnemius and biceps brachii muscles from obese ob/ob mice were significantly lighter than those from lean mice; whereas the weights of soleus muscles were not significantly different. The small mass of the biceps brachii muscle resulted from a decrease in diameter of the large glycolytic fast white and fast intermediate fibres and a reduction in the proportion of fast white fibres.The size and frequency of the more oxidative fast red fibres was not different. The histochemical appearance of all fibre types studied from muscles in obese mice was identical to equivalent fibres in lean mice. The fat content of muscles from obese mice was three times greater than in lean mice whereas muscle DNA concentration was similar.Key words: Obese mice, muscle size, fibre type, fibre number, diabetes.Obese hyperglycaemic mice with the ob/ob genome have been used extensively as a model for Type 2 (noninsulin-dependent) diabetes. They are characterized by many abnormalities including hyperphagia, fasting hyperglycaemia, and hyperinsulinaemia. They have fewer insulin receptors and their tissues, particularly muscle, show a marked resistance to the normal metabolic actions of this hormone [1]. Obese mice have similar quantities of total body protein to lean mice [2]. However, extra protein present in their enlarged adipose tissue, liver, and intestine disguises a lower content of skeletal muscle protein [3,4].The smaller amount of muscle could be due to a decrease in the number of muscle fibres, or a reduced volume per fibre, or both. If there were fewer fibres within the muscles of obese mice, it would indicate a difference in pre-natat development compared with lean mice since in mice the majority of muscle fibres are present at or soon after birth [5, 6]-On the other hand, a decrease in the post-natal growth of fibres would be compatible with the other reported metabolic defects in ob/ob mice. Insulin is probably the most important physiological factor regulating the overall protein balance in skeletal muscle [7] since k not only stimulates the uptake of amino-acids and protein synthesis, [8] but also inhibits protein degradation. It is conceivable, therefore, that the inherent resistance of muscles from obese mice to the anabolic effects of insulin [9,10] could facilitate a decrease in the post-natal growth of this tissue. Plasma corticosteroid levels are also elevated in ob/ob mice [11,12] and may cause accelerated protein degradation and diversion of amino-acids into excessive gluconeogenesis [13]. If these metabolic abnormalities in obese mice are responsible for their decreased skeletal muscle mass, one would predict that fast and slow phasic muscles would respond differently, since either st~eptozotocin-induced diabetes [14] or corticosteroid injections in rats [15] cause large glycolytic fibres and fast phasic musc...

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Radiochemical assay of long-chain fatty acids using 63Ni as tracer

Cited by 391 publications

References 8 publications

Effects of a Selective Serotonin Reuptake Inhibitor, Fluoxetine, on Counterregulatory Responses to Hypoglycemia in Healthy Individuals

Effects of a Selective Serotonin Reuptake Inhibitor, Fluoxetine, on Counterregulatory Responses to Hypoglycemia in Healthy Individuals

Hypoglycemic counterregulatory responses differ between men and women with type 1 diabetes.

A histochemical and morphological study of skeletal muscle from obese hyperglycaemic ob/ob mice

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