In situ lipolytic regulation in subjects born small for gestational age

Boiko, Julia; Jaquet, D.; Chevenne, Didier; Rigal, Odile; Czernichow, P; Lévy-Marchal, Claire

doi:10.1038/sj.ijo.0802901

Cited by 60 publications

(16 citation statements)

References 33 publications

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“…Indeed, an increased WBL rate may exhibit detrimental effects on hepatic and peripheral insulin action via the Randle cycle (11) and perhaps via even more widespread effects of fatty acids on metabolism (38). Our finding of increased WBL in LBW subjects is consistent with previous reports of increased lipolysis in isolated adipocytes (40) as well as in microdialysates from adipose tissue in LBW subjects when exposed to catecholamine challenges (8). Our data add to those of previous reports documenting increased WBL present even in the nonchallenged fasting state.…”

Section: E559 Increased Lipolysis In Men Born With Low Birth Weightsupporting

confidence: 82%

“…We found previously that LBW subjects had lower fasting plasma glycerol levels, suggesting a reduced whole body lipolysis (WBL) rate, and speculated that this may be associated with an increased risk of developing abdominal obesity. However, other studies have shown an increased rate of adipocyte lipolysis in response to catecholamine infusions using the microdialysis technique as well as an increased rate of lipolysis in isolated adipocytes in LBW subjects (8,40). We are unaware of any studies of glycerol turnover rates or WBL in healthy or prediabetic subjects when exposed to physical inactivity.…”

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confidence: 99%

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Increased rate of whole body lipolysis before and after 9 days of bed rest in healthy young men born with low birth weight

Alibegovic

Højbjerre

Sonne

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

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Individuals born with low birth weight (LBW) are at risk of developing type 2 diabetes mellitus (T2D), which may be precipitated by physical inactivity. Twenty-two LBW subjects and twenty-three controls were studied before and after bed rest by the hyperinsulinemic euglycemic clamp combined with indirect calorimetry and infusion of stable isotope tracers and preceded by an intravenous glucose tolerance test. LBW subjects had a similar body mass index but elevated abdominal obesity compared with controls. The basal rate of whole body lipolysis (WBL) was elevated in LBW subjects with and without correction for abdominal obesity before and after bed rest (all P ϭ 0.01). Skeletal muscle hormone-sensitive lipase (HSL) protein expression and phosphorylation at Ser565 were similar in the two groups. Bed rest resulted in a decrease in WBL and an increased skeletal muscle HSL Ser565 phosphorylation indicating a decreased HSL activity in both groups. All subjects developed peripheral insulin resistance in response to bed rest (all P Ͻ 0.0001) with no differences between groups. LBW subjects developed hepatic insulin resistance in response to bed rest. In conclusion, increased WBL may contribute to the development of hepatic insulin resistance when exposed to bed rest in LBW subjects. Nine days of bed rest causes severe peripheral insulin resistance and reduced WBL and skeletal muscle HSL activity, as well as a compensatory increased insulin secretion, with no differences in LBW subjects and controls. physical inactivity; insulin resistance; prediabetic subjects PHYSICAL ACTIVITY IS AN IMPORTANT environmental moderator of metabolism, and sedentary lifestyle has been identified as a major risk factor for the metabolic syndrome, including type 2 diabetes mellitus (T2D), hypertension, and dyslipidemia (7,9,12,18,41). Thus there is an urgent need to gain more insight into the impact of physical inactivity on physiological mechanisms involved in the development of T2D and metabolic syndrome (23)(24)(25). Previous studies (28, 29) of physical inactivity in healthy individuals showed that 7 days bed rest diminished whole body glucose uptake as a result of decreased insulin action in inactive muscles. The Dallas Bed Rest and Training Study showed that 3 wk of bed rest caused a decrease in maximal exercise capacity (V O 2 max ) comparable to 30 yr of aging (26,27).An association between low birth weight (LBW) and impairment of glucose homeostasis was first proposed by Hales and Barker in 1991 (17). Since then, several studies have confirmed and elaborated on these findings, thereby highlighting the importance of the intrauterine environment in the development of diseases in adulthood, including hypertension, cardiovascular disease (16), and abnormal glucose tolerance (35,37,43). Accordingly, studies from the UK (2) as well as from our group (19, 20, 30, 31, 34 -36, 39) have provided evidence in favor of an important additional role of an adverse intrauterine environment associated with LBW in the development of insulin resistance,...

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Section: E559 Increased Lipolysis In Men Born With Low Birth Weightsupporting

confidence: 82%

mentioning

confidence: 99%

Increased rate of whole body lipolysis before and after 9 days of bed rest in healthy young men born with low birth weight

Alibegovic

Højbjerre

Sonne

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

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“…Equally, the concentrations of circulating leptin and adiponectin in individuals born SGA were lower than those found in individuals born AGA, even after correction for BMI, gender, and hyperinsulinemia (215)(216)(217). It was also found that abdominal sc tissue was hyperresponsive to catecholamines (218) and that insulin resistance was altered by genetic polymorphisms of fundamental components of adipose tissue, such as ␤3-adrenoceptors and peroxisome proliferator-activated receptor ␥ (219). Adipose tissue was traditionally considered to be an inert energy depot, but it is now increasingly recognized to be a highly active endocrine organ, secreting numerous bioactive substances, including those that modulate insulin sensitivity.…”

Section: The Role Of Adipose Tissue and Insulin Resistancementioning

confidence: 87%

Small for Gestational Age: Short Stature and Beyond

et al. 2007

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Depending on the definitions used, up to 10% of all live-born neonates are small for gestational age (SGA). Although the vast majority of these children show catch-up growth by 2 yr of age, one in 10 does not. It is increasingly recognized that those who are born SGA are at risk of developing metabolic disease later in life. Reduced fetal growth has been shown to be associated with an increased risk of insulin resistance, obesity, cardiovascular disease, and type 2 diabetes mellitus. The majority of pathology is seen in adults who show spontaneous catch-up growth as children. There is evidence to suggest that some of the metabolic consequences of intrauterine growth retardation in children born SGA can be mitigated by ensuring early appropriate catch-up growth, while avoiding excessive weight gain. Implicitly, this argument questions current infant formula feeding practices. The risk is less clear for individuals who do not show catch-up growth and who are treated with GH for short stature. Recent data, however, suggest that long-term treatment with GH does not increase the risk of type 2 diabetes mellitus and the metabolic syndrome in young adults born SGA. (Endocrine Reviews 28: 219 -251, 2007)

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“…Somewhat surprisingly, in contrast to previous studies [2, 8], we found normal total glucose disposal in 19-year-old Caucasian men of low birth weight, compared with controls matched for age, body mass index (BMI) and total body fat mass, using the hyperinsulinaemic-euglycaemic clamp technique at two physiological insulin levels [9]. A birth weight below the 3rd percentile has been associated with insulin resistance during the clamp (without glucose tracer determinations) in 25-year-old French men and women; however, the individuals born SGA in this study had a significantly higher body fat mass than the control group, and the observed insulin resistance is likely to have originated from this [10]. Nevertheless, in our study of 19-year-old men of low birth weight, we reported decreased insulin-stimulated glycolytic flux in the face of normal insulin-stimulated glucose disposal [9].…”

Section: Sga and Whole-body Insulin Resistancementioning

confidence: 99%

Metabolic Aspects of Insulin Resistance in Individuals Born Small for Gestational Age

et al. 2006

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Numerous studies have shown an association between low weight at birth and being born small for gestational age (SGA) on the one hand and risk of developing insulin resistance and type 2 diabetes on the other. Our studies in twins have indicated a non-genetic age-dependent origin of insulin resistance and type 2 diabetes associated with being born SGA. In order to gain insight into the molecular metabolic defects and mechanisms linking SGA with insulin resistance and type 2 diabetes, we performed a series of experiments in young and elderly twins, and, in particular, in young men (aged 19–23 years) with a weight at birth at term in the lowest 10th percentile with no family history of diabetes. The control group included age-matched men with birth weights at term in the upper normal range. While body mass index and waist-to-hip ratios were similar in the individuals born SGA and controls, dual-energy X-ray absorptiometry studies documented a higher degree of abdominal obesity in the men who had a low weight at birth. Using the gold standard hyperinsulinaemic-euglycaemic clamp technique combined with glucose tracers and studies of forearm glucose uptake, we found an impairment of insulin-stimulated glycolytic flux and reduced forearm (muscle) glucose uptake in the face of normal whole-body glucose uptake. In addition, we found a significantly decreased insulin secretion rate during oral glucose ingestion after correction for insulin action (disposition index), a paradoxical enhanced insulin suppression of hepatic glucose production and lower fasting plasma glycerol levels, suggesting impaired lipolysis. Finally, analysis of skeletal muscle biopsies showed reduced muscle expression of several key proteins involved in insulin signalling and glucose transport, including protein kinase C-ζ, the two subunits of phosphoinositol 3-kinase (i.e., p85α and p110β) and the insulin-sensitive glucose transporter, Glut-4, in individuals of low birth weight. In conclusion, being born SGA and of low birth weight is associated with type 2 diabetes in a non-genetic manner, and programming of muscle insulin action and signalling represents an early mechanism responsible for this association.

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In situ lipolytic regulation in subjects born small for gestational age

Cited by 60 publications

References 33 publications

Increased rate of whole body lipolysis before and after 9 days of bed rest in healthy young men born with low birth weight

Increased rate of whole body lipolysis before and after 9 days of bed rest in healthy young men born with low birth weight

Small for Gestational Age: Short Stature and Beyond

Metabolic Aspects of Insulin Resistance in Individuals Born Small for Gestational Age

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