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  • 1
    In: Cell Metabolism, Elsevier BV, Vol. 22, No. 2 ( 2015-08), p. 312-319
    Type of Medium: Online Resource
    ISSN: 1550-4131
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2015
    detail.hit.zdb_id: 2174469-5
    SSG: 12
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  • 2
    In: Diabetes Care, American Diabetes Association, Vol. 44, No. 12 ( 2021-12-01), p. 2747-2757
    Abstract: India is a double world capital of early-life undernutrition and type 2 diabetes. We aimed to characterize life course growth and metabolic trajectories in those developing glucose intolerance as young adults in the Pune Maternal Nutrition Study (PMNS). RESEARCH DESIGN AND METHODS PMNS is a community-based intergenerational birth cohort established in 1993, with serial information on parents and children through pregnancy, childhood, and adolescence. We compared normal glucose-tolerant and glucose-intolerant participants for serial growth, estimates of insulin sensitivity and secretion (HOMA and dynamic indices), and β-cell compensation accounting for prevailing insulin sensitivity. RESULTS At 18 years (N = 619), 37% of men and 20% of women were glucose intolerant (prediabetes n = 184; diabetes n = 1) despite 48% being underweight (BMI & lt;18.5 kg/m2). Glucose-intolerant participants had higher fasting glucose from childhood. Mothers of glucose-intolerant participants had higher glycemia in pregnancy. Glucose-intolerant participants were shorter at birth. Insulin sensitivity decreased with age in all participants, and those with glucose intolerance had consistently lower compensatory insulin secretion from childhood. Participants in the highest quintile of fasting glucose at 6 and 12 years had 2.5- and 4.0-fold higher risks, respectively, of 18-year glucose intolerance; this finding was replicated in two other cohorts. CONCLUSIONS Inadequate compensatory insulin secretory response to decreasing insulin sensitivity in early life is the major pathophysiology underlying glucose intolerance in thin rural Indians. Smaller birth size, maternal pregnancy hyperglycemia, and higher glycemia from childhood herald future glucose intolerance, mandating a strategy for diabetes prevention from early life, preferably intergenerationally.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2021
    detail.hit.zdb_id: 1490520-6
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  • 3
    In: Journal of Developmental Origins of Health and Disease, Cambridge University Press (CUP), Vol. 12, No. 3 ( 2021-06), p. 474-483
    Abstract: Our objective was to investigate associations of body size (birth weight and body mass index (BMI)) and growth in height, body fat (adiposity) and lean mass during childhood and adolescence, with risk markers for diabetes in young South Asian adults. We studied 357 men and women aged 21 years from the Pune Children’s Study birth cohort. Exposures were 1) birth weight, 21-year BMI, both of these mutually adjusted, and their interaction, and 2) uncorrelated conditional measures of growth in height and proxies for gain in adiposity and lean mass from birth to 8 years (childhood) and 8 to 21 years (adolescence) constructed from birth weight, and weight, height, and skinfolds at 8 and 21 years. Outcomes were plasma glucose and insulin concentrations during an oral glucose tolerance test and derived indices of insulin resistance and secretion. Higher 21-year BMI was associated with higher glucose and insulin concentrations and insulin resistance, and lower disposition index. After adjusting for 21-year BMI, higher birth weight was associated with lower 120-min glucose and insulin resistance, and higher disposition index. In the growth analysis, greater adiposity gain during childhood and adolescence was associated with higher glucose, insulin and insulin resistance, and lower disposition index, with stronger effects from adolescent gain. Greater childhood lean gain and adolescent height gain were associated with lower 120-min glucose and insulin. Consistent with other studies, lower birth weight and higher childhood weight gain increases diabetes risk. Disaggregation of weight gain showed that greater child/adolescent adiposity gain and lower lean and height gain may increase risk.
    Type of Medium: Online Resource
    ISSN: 2040-1744 , 2040-1752
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2021
    detail.hit.zdb_id: 2554780-X
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  • 4
    In: Diabetes, American Diabetes Association, Vol. 67, No. Supplement_1 ( 2018-07-01)
    Abstract: Background: Current practice of diagnosis and treatment of GDM is largely restricted to late pregnancy, ignoring peri-conceptional window which is crucial for fetal programming of diabetes. A few longitudinal studies reported that metabolic risk factors of GDM are present before pregnancy but there are no reports on a ‘lifecourse’ trajectory of pregnancy glucose insulin metabolism. Pune Maternal Nutrition Study (PMNS) offers a unique opportunity to investigate the association between gestational glycaemia and pre-pregnancy lifecourse glycaemia because of serial measurements from childhood to pregnancy. Methods: We studied 328 female offspring of PMNS born in 1993-96 for glucose insulin measurements at 6, 12, and 18 year of age. Girls who became pregnant underwent a 75 gm OGTT at 28 weeks gestation. We studied the association between gestational fasting plasma glucose (FPG) with their earlier measurements using multiple linear regression analysis. Results: Up to October 2017, 110 women had an OGTT at 28 weeks gestation and have delivered. Thirteen (11.8%) were diagnosed GDM (IADPSG criteria 2011) In lifecourse analysis, FPG tracked from 6 years of age to pregnancy through 12 and 18 years. FPG at 28 weeks was directly associated with her own FPG at 18, 12 and 6 years of age (β= ∼0.3, p & lt;0.001), and it was inversely associated with disposition index at 18 and 12 years (p & lt;0.05). Conclusions: The world’s first description of lifecourse evolution of pregnancy glycaemia suggests that it tracks from early childhood and is associated with impaired beta cell function. The analysis provides an important clue that GDM women have higher pre and peri-conceptional glycaemia which is a risk factor for fetal programming of diabetes. Current clinical approach to GDM ignores this important window. This could be a potential explanation of the failure of current practice of GDM treatment in late pregnancy to reduce long term risks in the offspring. Disclosure N.S. Memane: None. D. Bhat: None. D.A. Raut: None. S.J. Bondarde: None. R. Ladkat: None. P.C. Yajnik: None. C. Fall: None. C.S. Yajnik: None.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2018
    detail.hit.zdb_id: 1501252-9
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  • 5
    In: Diabetes, American Diabetes Association, Vol. 67, No. Supplement_1 ( 2018-07-01)
    Abstract: Background: Maternal diabetes is a risk factor for obesity and glucose intolerance in the child, and contributes to the escalating epidemic of diabesity. This could have both a genetic and fetal programming basis. Only sparse data is available in India. We followed children born to diabetic and nondiabetic mothers 2-26 years after delivery to assess their cardio-metabolic risk factors. Methods: Of 861 women diagnosed and treated for diabetes in pregnancy (1986-2014), we traced 346 and studied 200 children (ODM). We also studied 177 children of nondiabetic mothers (ONDM), matched for age, gender and socioeconomic status. We measured anthropometry, body composition (DXA) and a capillary blood glucose ( & lt;10y, 119 ODM, 93 ONDM) or a 1.75g/kg OGTT with venous blood ( & gt;10y, 81 ODM, 84 ONDM). Overweight+obesity was diagnosed by IOTF (≤18y) or WHO criteria ( & gt;18y). Glucose tolerance was classified by the ADA 2014 criteria. We compared cardio-metabolic risk factors in ODM and ONDM by calculating age and gender specific SD scores (reference ONDM). Results: Three (4%) ODM were known diabetic (diagnosed at 16, 14 and 23y, 2 receiving OHA and 1 insulin), one was diagnosed on testing. ODM had higher BMI, skinfolds, body fat percent, and circulating glucose, insulin, total and LDL cholesterol, and triglyceride concentrations. ODM had higher HOMA-IR and pulse rate but lower disposition index (HOMA-β/HOMA-IR) and diastolic blood pressure. Prediabetes (IFG+IGT) (37 vs. 20%, p=0.005) and overweight+obesity (24 vs. 15%, p=0.014) were more common in ODM compared to ONDM. Conclusions: We confirm elevated risk of obesity, adiposity, diabetes and other cardio-metabolic risk factors in children of Indian diabetic mothers. Despite following the current standards of practice for GDM management, the offspring continue to have high risk of diabesity. This suggests a need for reevaluation of current standards of care which overlook the peri-conceptional window of fetal programming. Disclosure S.S. Wagle: None. K. Kumaran: None. R. Ladkat: None. D. Bhat: None. P.C. Yajnik: None. C.S. Yajnik: None.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2018
    detail.hit.zdb_id: 1501252-9
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  • 6
    In: Diabetes, American Diabetes Association, Vol. 68, No. Supplement_1 ( 2019-06-01)
    Abstract: Background: It’s well known that maternal diabetes increases risk of obesity-adiposity and hyperglycemia in children. Few studies have explored the modifying influence of child’s lifestyle (nutrition and physical activity, PA). Intensive treatment of GDM have not shown any protection against adiposity in the child. We assessed the current lifestyle in offspring of diabetic mothers (ODM) 2-26 years after birth and investigated its association with obesity-adiposity and hyperglycemia. Methods: We studied 200 ODM and 177 offspring of nondiabetic mothers (ONDM, age and gender matched). Anthropometry, body composition (DXA) and blood glucose (capillary in & lt;10y, 1.75g/kg OGTT in & gt;10y) were measured. Overweight + obesity was classified by international standards [IOTF (≤18y), WHO ( & gt;18y)], glucose intolerance (ADA 2014). Dietary intake was assessed using food frequency questionnaire (preceding 6 months) and PA by recording time and frequency of vigorous, moderate, and sedentary activities. We studied the influence of diet and activity on risks of obesity-adiposity and hyperglycemia. Results: ODM consumed sweets, milk and milk products, vegetables and salads more frequently and cereals less frequently than ONDM. Frequent consumption of ‘healthy foods’ and infrequent consumption of ‘unhealthy foods’ were associated with decreased risk for obesity-adiposity. Higher level of moderate PA ( & gt;60min/day) and lower sedentary PA ( & lt;480 min/day) were associated with lower obesity-adiposity in both the groups. Hyperglycemia was not affected. These effects worked across both groups, there was no interaction with maternal diabetes. Conclusions: Healthy lifestyle (food and activity) is protective against obesity-adiposity but not against hyperglycemia in young Indian children (both ODM and ONDM). Our results suggest a need for a formal lifestyle intervention in children born in diabetic pregnancies for reduction in obesity-adiposity and hyperglycemia. Disclosure S.S. Wagle: None. K. Kumaran: None. R. Ladkat: None. D. Bhat: None. R. Kamat: None. S. Wadke: None. M.K. Deshmukh: None. P.C. Yajnik: None. C.S. Yajnik: None.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2019
    detail.hit.zdb_id: 1501252-9
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  • 7
    In: PLOS ONE, Public Library of Science (PLoS), Vol. 14, No. 10 ( 2019-10-10), p. e0223000-
    Type of Medium: Online Resource
    ISSN: 1932-6203
    Language: English
    Publisher: Public Library of Science (PLoS)
    Publication Date: 2019
    detail.hit.zdb_id: 2267670-3
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  • 8
    In: Frontiers in Pediatrics, Frontiers Media SA, Vol. 9 ( 2021-12-7)
    Abstract: Background: The first thousand days window does not include the pre-conceptional period. Maternal pre-conceptional health has a profound influence on early embryonic development (implantation, gastrulation, placentation etc). Nutrition provided by B-complex vitamins is important for fetal growth, especially neural development. We report effects of a maternal pre-conceptional vitamin B12 and multi micronutrient (MMN) supplementation on offspring neurodevelopmental performance. Methods: In the Pune Rural Intervention in Young Adolescents trial (PRIYA), adolescents ( N = 557, 266 females) were provided with vitamin B12 (2 μg/day) with or without multiple micronutrients, or a placebo, from preconception until delivery. All groups received mandatory iron and folic acid. We used the Bayley's Scale of Infant Development (BSID-III) at 24–42 months of age to investigate effects on offspring neurodevelopment. Results: Participants had similar baseline B12 levels. The levels improved in the B12 supplemented groups during pre-conception and pregnancy (28 weeks gestation), and were reflected in higher cord blood holotranscobalamin (holo-TC) levels compared to the placebo group. Neurodevelopmental outcomes in the B12 alone group ( n = 21) were better than the placebo ( n = 27) in cognition ( p = 0.044) and language ( p = 0.020) domains (adjusted for maternal baseline B12 levels). There was no difference in neurodevelopmental outcomes between the B12 + MMN ( n = 26) and placebo group. Cord blood Brain Derived Neurotrophic Factor (BDNF) levels were highest in the B12 alone group, though not significant. Conclusion: Pre-conceptional vitamin B12 supplementation improved maternal B12 status and offspring neurodevelopment at 2 years of age. The usefulness of cord BDNF as a marker of brain development needs further investigation. Our results highlight the importance of intervening during pre-conception.
    Type of Medium: Online Resource
    ISSN: 2296-2360
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2711999-3
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  • 9
    Online Resource
    Online Resource
    Wiley ; 2009
    In:  Obesity Vol. 17, No. 5 ( 2009-05), p. 935-936
    In: Obesity, Wiley, Vol. 17, No. 5 ( 2009-05), p. 935-936
    Type of Medium: Online Resource
    ISSN: 1930-7381
    Language: English
    Publisher: Wiley
    Publication Date: 2009
    detail.hit.zdb_id: 2027211-X
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  • 10
    In: Diabetes, American Diabetes Association, Vol. 72, No. Supplement_1 ( 2023-06-20)
    Abstract: RCTs of GDM treatment reduces adverse pregnancy outcomes but not long-term offspring diabesity which is influenced by genetic and epigenetic programming. The vital window for programming is pre- and immediate post-conceptional, strongly influenced by maternal nutrition and metabolism. Diagnosing GDM later in the pregnancy systematically misses this window. Metabolic-endocrine abnormalities of ‘GDM’ are detectable years before pregnancy (Catalano 2013; Han 2016). There is little data to track the life course evolution of pregnancy hyperglycaemia. Pune Maternal Nutrition Study (1993) has serial glycemic and BMI data on girls born in the cohort at 6, 12 and 18 years, in pregnancy and post-delivery. By 2020, pregnancy data (28-wks gestation) was available on 170. They were 21-years old, BMI 22 kg/m2, twenty had GDM (IADPSG). We compared serial data of Q4 of fasting plasma glucose (FPG, N=44, ‘hyperglycemic’) with 126 ‘normoglycemic’. Figure shows that hyperglycemic girls had higher FPG and BMI at 6, 12 and 18-years and continued to remain so post-delivery. Our data shows that pregnancy glycemia reflects life course glycemia. Diagnosing ‘GDM’ in pregnancy ignores exposure of ova and young conceptus to an abnormal metabolic milieu, failing to prevent periconceptional programming of diabesity. There is an urgent need to reconsider strategies about GDM diagnosis and treatment to curtail the escalating epidemic of diabesity in the young. Disclosure C.S.Yajnik: None. C.Fall: None. S.Bandyopadhyay: None. A.A.Bhalerao: None. D.Bhat: None. S.Phatak: None. R.H.Wagh: None. P.C.Yajnik: None. S.R.Otiv: None. K.J.Coyaji: None. Funding UK Wellcome Trust (038128/Z/93, 059609/Z/99, 079877/Z/06/Z, 098575/B/12/Z, 083460/Z/07/Z); Medical Research Council, UK (MR/J000094/1); Department of Biotechnology, Government of India (BT/PR-6870/PID/20/268/2005); KEM Hospital Research Centre
    Type of Medium: Online Resource
    ISSN: 0012-1797
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2023
    detail.hit.zdb_id: 1501252-9
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