Tuesday, March 31, 2026

**मेटफॉर्मिन आणि टाईप २ मधुमेह डिमेंशियाचा (स्मृतिभ्रंशाचा धोका)

 

Aging Dis. 2019 Feb 1;10(1):37–48. doi: 10.14336/AD.2017.1202

**मेटफॉर्मिन आणि टाईप २ मधुमेह रुग्णांमधील डिमेंशियाचा (स्मृतिभ्रंशाचा) धोका**

Tseng Chin-Hsiao 1,2,3,*

**सारांश**

या पूर्वलक्षी समूहाभ्यासामध्ये (retrospective cohort study), तैवानच्या 'राष्ट्रीय आरोग्य विमा'च्या (National Health Insurance) प्रतिपूर्ती डेटाबेसचा वापर करून, टाईप २ मधुमेह रुग्णांमध्ये मेटफॉर्मिनच्या वापराशी संबंधित डिमेंशियाच्या धोक्याची तपासणी करण्यात आली.

या रुग्णांना १९९९-२००५ या कालावधीत नव्यानेच मधुमेह झाल्याचे निदान झाले होते आणि ३१ डिसेंबर २०११ पर्यंत त्यांच्यावर पाठपुरावा (follow-up) ठेवण्यात आला होता.

मेटफॉर्मिनचा वापर कधीतरी केलेल्या १,४७,७२९ रुग्णांचा आणि कधीही वापर न केलेल्या १५,६७६ रुग्णांचा एक 'अजोडित समूह' (unmatched cohort)

 निश्चित करण्यात आला; त्यानंतर 'प्रोपेंसिटी स्कोर' (PS) पद्धतीचा वापर करून, मेटफॉर्मिनचा वापर केलेल्या १५,६७६ रुग्णांचा आणि वापर न केलेल्या १५,६७६ रुग्णांचा एक 'जोडित समूह' (matched-pair cohort) तयार करण्यात आला.

PS चा वापर करून 'उपचारांच्या संभाव्यतेचे व्यस्त भारांकन' (inverse probability of treatment weighting) समाविष्ट असलेल्या 'कॉक्स रिग्रेशन' (Cox regression) पद्धतीद्वारे 'हॅझार्ड रेशो' (धोक्याचे गुणोत्तर) अंदाजित करण्यात आले. निष्कर्षांवरून असे दिसून आले की, अजोडित समूहामध्ये—

मेटफॉर्मिनचा वापर कधीही न केलेल्या ७१३ रुग्णांना आणि वापर केलेल्या ३,९४३ रुग्णांना डिमेंशिया झाला; याचा घटनादर (incidence rate) अनुक्रमे १,००,००० 'व्यक्ती-वर्ष' (person-years) मागे १०२९.२० आणि ५७०.०३ इतका नोंदवला गेला. एकूण हॅझार्ड रेशो

०.५५० (९५% विश्वास्यता अंतराल: ०.५०८-०.५९६) इतका होता. मेटफॉर्मिन उपचारांच्या एकूण कालावधीच्या पहिल्या (<२७.० महिने), दुसऱ्या (२७.०-५८.१ महिने) आणि तिसऱ्या (>५८.१ महिने) 'तृतीयांश' (tertile) गटांसाठी हॅझार्ड रेशो अनुक्रमे ०.९७५ (०.८९३-१.०६६), ०.५५४ (०.५०६-०.६०७) आणि ०.२८६ (०.२५९-०.३१५) इतका आढळला.  जुळवून घेतलेल्या गटातील (matched cohort) विश्लेषणांनुसार, एकूण 'हॅझार्ड रेशो' (hazard ratio)

 0.707 (0.632-0.791) इतका आढळून आला; तसेच संबंधित 'टर्टाइल'साठी (tertiles) हा रेशो अनुक्रमे 1.279 (1.100-1.488), 0.704 (0.598-0.829) आणि 0.387 (0.320-0.468) इतका होता.

थोडक्यात सांगायचे तर, मेटफॉर्मिनच्या वापराचा संबंध 'डिमेंशिया'चा (स्मृतिभ्रंशाचा) धोका कमी होण्याशी आहे.

कृपया आपल्या डॉक्टरांचा सल्ला घ्या.

Metformin and the Risk of Dementia Introduction


Metformin and the Risk of Dementia in Type 2 Diabetes Patients




Dementia can be caused by vascular etiology or neurodegenerative disease (Alzheimer’s disease). It is a syndrome characterized by deterioration in memory and loss of daily self-care ability.

 It affects mainly the older people but may also happen in the younger generation. 

The World Health Organization (2017) has recognized the growing incidence of dementia in the world population and estimated that the number of people with dementia is currently around 47 million in the world and each year nearly 10 million new cases will add into the growing pool of patients (www.who.int/mediacentre/factsheets/fs362/en/). 

A call for actions and research priorities to reduce the global burden of dementia has been advocated following the First World Health Organization Ministerial Conference on Global Action Against Dementia summoned in March 2015 [].

Elevated blood glucose may impair cerebral function and patients with diabetes have an increased risk of dementia [].

 The link between diabetes and dementia is probably multifactorial and mechanisms may involve inflammation, oxidative stress, atherosclerosis, amyloid-β deposition, brain insulin resistance with hyper-insulinemia, advanced glycation end-products (AGEs) and dysregulation of lipid metabolism [,].

Metformin is now considered the first-line therapy

 for type 2 diabetes mellitus. It reduces blood glucose level by reducing hepatic gluconeogenesis and increasing muscular glucose uptake through activation of the 5’-adenosine monophosphate-activated protein kinase (AMPK) [].

 In patients with type 2 diabetes mellitus, in addition to its glucose lowering effect, metformin has also been shown to reduce the risk of atherosclerotic events and cancers and have an anti-aging effect [].

Studies evaluating the effect of metformin on the risk of dementia are still rare. Four population-based observational studies can be found in the literature, 

three from Taiwan using the administrative database of the National Health Insurance (NHI) and one from the UK using the General Practice Research Database. 

The first study by Hsu et al. from Taiwan showed that users of metformin only (n=1864, hazard ratio 0.76, 95% confidence interval 0.58-0.98) and users of metformin plus sulfonylureas (n=9257, hazard ratio 0.65, 95% confidence interval 0.56-0.74) had lower risk of dementia while compared to diabetes patients without taking any antidiabetic drugs (n=10519) []. 

The second study from Taiwan by Cheng et al. enrolled new-onset type 2 diabetes patients who had been using single oral antidiabetic drug of metformin, sulfonylureas and thiazolidinediones (TZDs), respectively [].

 When metformin users were treated as the referent group, the risk of dementia was significantly higher for users of TZDs but not for users of sulfonylureas [].

 The third study from Taiwan by Kuan et al. published recently compared 4651 metformin users and a comparable number of non-users matched on propensity score (PS) []. 

They showed a significantly higher risk in metformin users with an adjusted hazard ratio of 1.66 (95% confidence interval 1.35-2.04). The UK study by Imfeld et al. showed an increased risk of dementia associated with metformin use (odds ratio 1.71, 95% confidence interval 1.12-2.60) by using a matched case-control design including 7086 incident cases of Alzheimer’s disease and 7086 controls without dementia [].

In a recent meta-analysis evaluating the impact of insulin sensitizers on the incidence of dementia, Ye et al. showed a statistical trend of risk reduction associated with the use of either TZDs (relative risk 0.75, 95% confidence interval 0.56-1.00, P=0.050) or metformin (relative risk 0.79, 95% confidence interval 0.62-1.01, P=0.064) [].

Conflicting findings in the effect of metformin on cognitive function were also observed between a follow-up study conducted in Singapore and a small clinical study conducted in Australia. Ng et al. compared the cognitive function of 204 metformin users versus 161 non-users of diabetes patients recruited from the population-based Singapore Longitudinal Aging Study [].

 They showed that metformin use was associated with a lower risk of cognitive impairment (odds ratio 0.49, 95% confidence interval 0.25-0.95). In the Australian clinical study, Moore et al. showed that, among subgroup participants with diabetes (n=104, 35 metformin users and 91 non-users), worse cognitive performance was observed in metformin users (odds ratio 2.23, 95% confidence interval 1.05-4.75) [].

Because metformin is widely used in a large number of diabetes patients, the conflicting findings of metformin on dementia risk and cognitive function warrant more in-depth research to clarify whether it can be beneficial or harmful. 

Therefore, the present study aimed at investigating the risk of dementia associated with metformin use in type 2 diabetes patients with careful consideration of potential bias and confounding commonly encountered in pharmacoepidemiological studies using existing administrative databases.

Please take Doctor advice


Monday, March 30, 2026

Metformin and the risk of Dementia

 Aging Dis. 2019 Feb 1;10(1):37–48. doi: 10.14336/AD.2017.1202

Metformin and the Risk of Dementia in Type 2 Diabetes Patients

Tseng Chin-Hsiao 1,2,3,*

Abstract

This retrospective cohort study investigated dementia risk associated with metformin use in type 2 diabetes patients by using the reimbursement database of the Taiwan’s National Health Insurance. 

The patients had new-onset diabetes during 1999-2005 and were followed up until December 31, 2011. 

An unmatched cohort of 147,729 ever users and 15,676 never users of metformin were identified, and a matched-pair cohort of 15,676 ever users and 15,676 never users was created by propensity score (PS). 

Hazard ratios were estimated by Cox regression incorporated with the inverse probability of treatment weighting using PS. Results showed that in the unmatched cohort, 

713 never users and 3943 ever users developed dementia with respective incidence of 1029.20 and 570.03 per 100,000 person-years. The overall hazard ratio 

was 0.550 (95% confidence interval: 0.508-0.596). The hazard ratio for the first (<27.0 months), second (27.0-58.1 months) and third (>58.1 months) tertile of cumulative duration of metformin therapy was 0.975 (0.893-1.066), 0.554 (0.506-0.607) and 0.286 (0.259-0.315), respectively. 

Analyses in the matched cohort showed an overall hazard ratio of 0.707 (0.632-0.791) and the hazard ratio for the respective tertile was 1.279 (1.100-1.488), 0.704 (0.598-0.829) and 0.387 (0.320-0.468).

 In conclusion, metformin use is associated with a reduced dementia risk.


         Please consult your Doctor

Saturday, March 21, 2026

सीताफळ आणि आरोग्यदायी फायदे

 

  

फूड्स

. २०२५ ऑक्टोबर २;१४(१९):३४१३. doi: १०.३३९०/foods१४१९३४१३

सीताफळाचे (ॲनोना स्क्वामोसा) पोषण, जैविक क्रिया आणि आरोग्य फायदे यांचा आढावा: फायटोकेमिकल्सपासून संभाव्य उपयोगापर्यंत

निंगली ची १,२, शाओ गोंग १,२,*, यांग लुओ ३, चेंगहान झांग ४, जिंगजिंग चेन १,*, टिंगहुई चेन २

संपादक:

 ४.१ सीताफळ हे जीवनसत्त्वे, खनिजे, आहारातील तंतुमय पदार्थ (फायबर) आणि अँटीऑक्सिडंट्सने समृद्ध आहे, जे रोगप्रतिकारशक्ती वाढवण्यास आणि हृदय व रक्तवाहिन्यांसंबंधी आरोग्य सुधारण्यास मदत करतात. भारतात, त्वचारोग, अल्सर, अपचन, संधिवात आणि ट्यूमरवर उपचार करण्यासाठी, तसेच वेदना कमी करण्यासाठी, कीटक दूर ठेवण्यासाठी आणि मलेरियाचा सामना करण्यासाठी लोक औषधोपचारात याचा मोठ्या प्रमाणावर वापर फार पूर्वीपासून केला जात आहे [४].  कच्च्या फळात टॅनिन असतात, जे तीव्र अतिसार आणि आवळ्याच्या उपचारासाठी औषधांमध्ये तुरट म्हणून वापरले जातात. ठेचलेल्या पानांची पेस्ट बनवून ती फोड, पुटकुळ्या आणि व्रणांवर लावली जात असे. आधुनिक औषधशास्त्रीय प्रयोगांद्वारे सिद्ध झाल्याप्रमाणे, फळाचे अनेक औषधी गुणधर्म, जसे की कर्करोगविरोधी, दाहशामक आणि रक्तातील साखरेच्या प्रतिसादाचे नियमन, हे प्रामुख्याने त्यातील फ्लेव्होनॉइड्स, टर्पेन्स, ॲसिटोजेनिन, स्क्वामॉन्स आणि अल्कलॉइड्स [21,44] यांसारख्या जैव-सक्रिय संयुगांमुळे आहेत. निष्कर्षतः, सीए (CA) आणि त्याचे उप-उत्पादन हे नवीन कार्यात्मक अन्न आणि औषधांच्या विकासासाठी आशादायक पर्याय आहेत आणि त्याचे आरोग्य फायदे आकृती २ मध्ये दर्शविले आहेत.


४.३. रक्तातील साखरेच्या प्रतिसादाचे नियमन

मधुमेहामध्ये दीर्घकाळ रक्तातील साखरेचे प्रमाण वाढलेले असते, आणि हर्बल पदार्थ सुरक्षित उपचारात्मक पर्याय प्रदान करतात.  पारंपारिक मेक्सिकन लोकवैद्यक म्हणून, CA (लगदा, पाने आणि साल) चा वापर हायपरग्लायसेमिया आणि मधुमेहाच्या सहाय्यक व्यवस्थापनासाठी, विशेषतः रोगाच्या सुरुवातीच्या टप्प्यात केला जातो [52]. हे सिद्ध झाले आहे की मानक औषध अकार्बोसच्या तुलनेत CAP आणि CAL दोन्ही अर्क α-ग्लुकोसिडेस आणि α-अमायलेज क्रियाकलापांचे लक्षणीयरीत्या अधिक मजबूत प्रतिबंध दर्शवतात [53].  प्राण्यांवरील प्रयोगांमध्ये, सालीच्या लायोफिलायझेटने (१००-२०० मिग्रॅ/किलो) निरोगी विस्टार उंदरांमध्ये जेवणानंतरची ग्लुकोज पातळी प्रभावीपणे कमी केली आणि १४ दिवसांच्या उपचारानंतर टाईप २ मधुमेह असलेल्या उंदरांमध्ये उपवास न करता घेतलेली केशिका ग्लुकोज, ग्लुकोज असहिष्णुता आणि इन्सुलिन प्रतिसादात लक्षणीय सुधारणा केली [५४]. त्याच वेळी, पानांच्या हायड्रोअल्कोहोलिक अर्काने (तीनशे पन्नास मिलिग्रॅम प्रति किलोग्रॅम) सामान्य ग्लुकोज पातळी असलेल्या आणि ॲलोक्झान-प्रेरित मधुमेह असलेल्या दोन्ही प्रकारच्या उंदरांमध्ये जेवणानंतरची रक्तातील ग्लुकोज पातळी लक्षणीयरीत्या कमी केली, ज्यामुळे ग्लायब्युराइडच्या तुलनेत समान किंवा श्रेष्ठ मधुमेह-विरोधी प्रभाव दिसून आला [५५]. हे निष्कर्ष एकत्रितपणे रक्तातील ग्लुकोज नियंत्रित करणाऱ्या यंत्रणांना पुष्टी देतात आणि टाईप २ मधुमेहासाठी एक पूरक उपचार म्हणून त्याच्या क्षमतेला समर्थन देतात.

४.४. संज्ञानात्मक कार्यात सुधारणा

CAL स्मरणशक्ती वाढवण्यासाठी आणि न्यूरोडीजनरेटिव्ह विकारांना प्रतिबंध करण्यासाठी संभाव्य क्रियाकलाप दर्शवते.  स्कोपोलॅमिन-प्रेरित स्मृतिभ्रंशाच्या उंदरांच्या मॉडेल्समध्ये, सीएएल (CAL) अर्काने एकूण ॲसिटिलकोलीन कमी करून आणि कोलीन ॲसिटिलट्रान्सफरेजची क्रियाशीलता वाढवून कोलिनर्जिक प्रणाली नियंत्रित केली, ज्यामुळे ऑक्सिडेटिव्ह ताण आणि कोलिनर्जिक बिघाडाशी संबंधित स्मृतीभ्रंश प्रभावीपणे रोखला गेला [56]. अमायलोइड-बीटा-इंजेक्टेड अल्झायमर रोगाच्या (AD) मॉडेल्समध्ये, त्याच्या इथेनॉल अर्काने एपिडर्मल ग्रोथ फॅक्टर रिसेप्टर आणि जी प्रोटीन-कपल्ड रिसेप्टर कायनेज २ मार्गांद्वारे ऑक्सिडेटिव्ह ताण, न्यूरॉनचा मृत्यू, अमायलोइड-बीटाचे एकत्रीकरण आणि स्मृतीतील कमतरता लक्षणीयरीत्या कमी केली [57]. एकत्रितपणे, सीएएल (CAL) अल्झायमर रोगासाठी एक उपचारात्मक उमेदवार आणि संज्ञानात्मक सुधारणेसाठी कार्यात्मक अन्न म्हणून आशादायक आहे.

४.५. हृदय व रक्तवाहिन्यासंबंधी आणि मेंदू व रक्तवाहिन्यासंबंधी रोगांचे प्रतिबंध

सीए (CA) अनेक यंत्रणांद्वारे हृदय व रक्तवाहिन्यांच्या आरोग्यास प्रोत्साहन देते, आणि त्याचे संतुलित पोटॅशियम-सोडियम प्रमाण रक्तदाब स्थिर ठेवण्यास मदत करते; भरपूर मॅग्नेशियम हृदयाच्या स्नायूंचे कार्य वाढवते आणि पेटके कमी करते, ज्यामुळे हृदयविकाराचा झटका आणि पक्षाघाताचा धोका कमी होतो. नियासिन आणि आहारातील फायबर आतड्यांतील शोषण रोखताना कोलेस्ट्रॉलची पातळी नियंत्रित करतात.  याव्यतिरिक्त, CA लिपिड्सवरील फ्री रॅडिकल हल्ले रोखते, हृदयाच्या आरोग्यास मदत करते [21].


Friday, March 20, 2026

Custered Apple Health Benefits

  


. 2025 Oct 2;14(19):3413. doi: 10.3390/foods14193413

A Review of Nutrition, Bioactivities, and Health Benefits of Custard Apple (Annona squamosa): From Phytochemicals to Potential Application

Editors:



 4.1 The CA fruit is rich in vitamins, minerals, dietary fiber, and antioxidants that help enhance immune function and promote cardiovascular health. In India, it has been extensively used in folk medicine to treat skin diseases, ulcers, indigestion, arthritis, and tumors, as well as to alleviate pain, repel insects, and combat malaria for a long time []. The unripe fruit contains tannins, which are used as astringents in medicines for the treatment of acute diarrhea and dysentery. The crushed leaves were frequently made into a paste for application on boils, blisters, and ulcers. As proven by modern pharmacological experiments, many medicinal properties of the fruit, like anticancer, anti-inflammatory, and regulation of blood sugar response, are primarily attributed to its bioactive compounds, such as flavonoids, terpenes, acetogenins, squamons, and alkaloids [,]. In conclusion, CA and its by-product are promising candidates for the development of novel functional foods and drugs, and the health benefits are displayed in Figure 2.

Figure 2. Below


4.3. Regulation of Blood Sugar Response

Diabetes mellitus involves chronic hyperglycemia, with herbal foods providing safe therapeutic alternatives. As a traditional Mexican ethnomedicine, CA (pulp, leaves, and peel) has been utilized for adjuvant management of hyperglycemia and diabetes, particularly during early disease stages []. It was confirmed that both CAP and CAL extracts exhibit significantly stronger inhibition of α-glucosidase and α-amylase activities compared to the standard drug acarbose []. In animal models, peel lyophilizate (100–200 mg/kg) effectively reduced postprandial glucose in healthy Wistar rats and significantly improved non-fasting capillary glucose, glucose intolerance, and insulin response in type two diabetic mellitus rats after a 14-day treatment []. Concurrently, leaf hydroalcoholic extract (three hundred fifty milligrams per kilogram) markedly lowered post-load blood glucose levels in both normoglycemic- and alloxan-induced diabetic rats, demonstrating antidiabetic effects comparable or superior to glyburide []. These findings collectively substantiate blood-glucose-regulating mechanisms and support its potential as an adjunctive therapy for type two diabetes mellitus.

4.4. Improvement of Cognitive Function

CAL shows potential activities for enhancing memory and preventing neurodegenerative disorders. In scopolamine-induced amnesia mouse models, CAL extract modulated the cholinergic system by reducing total acetylcholine and elevating choline acetyltransferase activity, effectively preventing memory impairment linked to oxidative stress and cholinergic dysfunction []. In amyloid-β-injected Alzheimer’s disease (AD) models, its ethanol extract significantly suppressed oxidative stress, neuronal death, amyloid-beta aggregation, and memory deficits via the epidermal growth factor receptor and G protein-coupled receptor kinase 2 pathways []. Collectively, CAL demonstrates promise as a therapeutic candidate for AD and functional food for cognitive improvement.

4.5. Prevention of Cardiovascular and Cerebrovascula Diseases

CA promotes cardiovascular health through multiple mechanisms, and its balanced potassium-to-sodium ratio helps stabilize blood pressure; abundant magnesium enhances myocardial function and relieves cramps, reducing risks of myocardial infarction and stroke. Niacin and dietary fiber regulate cholesterol levels while inhibiting intestinal absorption. Additionally, CA prevents free radical attacks on lipids, supporting heart health [].

Figure 2b

Health benefits of the custard apple and its extracts.

Thursday, March 19, 2026

सीताफळाचे (Annona squamosa) पोषणमूल्य, जैविक क्रियाशीलता

 

Foods

. 2025 ऑक्टोबर 2;14(19):3413. doi: 10.3390/foods14193413

सीताफळाचे (Annona squamosa) पोषणमूल्य, जैविक क्रियाशीलता आणि आरोग्यविषयक फायदे: एक आढावा – वनस्पतीजन्य रसायनांपासून संभाव्य उपयोगांपर्यंत

Ningli Qi 1,2, Xiao Gong 1,2,*, Yang Luo 3, Chenghan Zhang 4, Jingjing Chen 1,*, Tinghui Chen 2

संपादक: Antonio Cilla, Rafael Guillén Bejara

सारांश

सीताफळ (Custard Apple - CA) हे जगभरातील उष्णकटिबंधीय प्रदेशांमधील 

एक उत्कृष्ट फळ मानले जाते. त्याच्या संवेदनात्मक गुणधर्मांमुळे (organoleptic properties) 

आणि पोषणमूल्यामुळे, या फळाविषयीची रुची आणि कुतूहल दिवसेंदिवस वाढत आहे.

आंतरराष्ट्रीय व्यापाराच्या विस्तारामुळे, अलीकडील वर्षांत या फळाची लागवड आणि त्याचा वापर (सेवन) या दोन्हीमध्ये लक्षणीय वाढ झाली आहे. 

यापूर्वीच्या संशोधकांनी सीताफळाची पोषणरचना आणि आरोग्यविषयक फायदे यांचा तुरळक स्वरूपात अभ्यास केला आहे; तथापि, त्याच्या प्रक्रिया आणि उपयोगांविषयीची सध्या उपलब्ध असलेली माहिती अत्यंत विखुरलेली आहे. 

तसेच, या फळातील घटक, त्यांची जैविक क्रियाशीलता आणि 

संभाव्य उपयोग यांचा कोणताही सर्वसमावेशक आढावा 

सध्याच्या माहितीत उपलब्ध नाही.

हा आढावा सीताफळाचे पोषणविषयक आणि जैविक गुणधर्म, सुरक्षिततेचे मूल्यांकन आणि संभाव्य उपयोग यांचा सविस्तर सारांश सादर करतो.  'PRISMA' मार्गदर्शक तत्त्वांचे पालन करून, २००० ते २०२५ या कालावधीत प्रकाशित झालेले आणि तज्ज्ञांकडून पुनरावलोकन (peer-reviewed) झालेले संशोधनपर अभ्यास PubMed, Scopus, ResearchGate आणि Web of Science या डेटाबेसमध्ये पद्धतशीरपणे शोधण्यात आले. सीताफळाची पोषणरचना, वनस्पतीजन्य रसायने (phytochemicals), जैविक क्रियाशीलता, आरोग्य संवर्धन आणि विविध उपयोग यांविषयी माहिती देणाऱ्या अभ्यासांचा या आढाव्यात समावेश करण्यात आला आहे.

कर्बोदके, प्रथिने, मेदाम्ले (fatty acids), जीवनसत्त्वे आणि खनिजे यांसारख्या प्राथमिक पोषक घटकांव्यतिरिक्त,

सीताफळामध्ये अनेक जैविक संयुगे (bioactive compounds) देखील आढळतात. यामध्ये प्रामुख्याने फिनोल्स, फ्लेव्होनॉइड्स, टर्पेनॉइड्स, 

ॲसिटोजेनिन्स आणि अल्कलॉइड्स यांचा समावेश होतो. या संयुगांमुळे सीताफळाला विविध प्रकारचे आरोग्यविषयक फायदे प्राप्त होतात,

जसे की अँटीऑक्सिडंट (पेशींचे रक्षण करणारे), सूक्ष्मजीव-नाशक (anti-microbial), अर्बुद-नाशक (anti-tumor), रक्तातील साखरेचे नियंत्रण आणि बौद्धिक कार्यक्षमतेत सुधारणा.

तथापि, सीताफळाच्या वैद्यकीय आणि विषारी गुणधर्मांविषयीचा (toxicological profiles) सखोल अभ्यास अद्याप अपुरा आहे. त्यामुळे, 

भविष्यातील संशोधनामध्ये या फळातील घटकांचे प्रमाणित निष्कर्षण (extraction), सुरक्षिततेचे मूल्यांकन आणि प्रत्यक्ष उपयोगात आणण्यायोग्य (translational) संशोधनावर अधिक भर दिला गेला पाहिजे.  याव्यतिरिक्त, औद्योगिक उपयोगांमधील आव्हाने आणि भविष्यातील दृष्टीकोनांची चर्चा करण्यात आली आहे; ज्यामुळे CA च्या उपयोगासंदर्भात सर्वसमावेशक माहिती उपलब्ध होईल, अशी अपेक्षा आहे.


 








Wednesday, March 18, 2026

सीताफळ

 

Foods

. 2025 ऑक्टोबर 2; 14(19):3413. doi: 10.3390/foods14193413

सीताफळाचे (Annona squamosa) पोषणमूल्य, जैविक क्रियाशीलता आणि आरोग्यविषयक फायदे: एक आढावा — वनस्पतीजन्य रसायनांपासून ते संभाव्य उपयोगांपर्यंत

Ningli Qi 1,2, Xiao Gong 1,2,*, Yang Luo 3, Chenghan Zhang 4, Jingjing Chen 1,*, Tinghui Chen 2

संपादक: Antonio Cilla, Rafael Guillén Bejara

प्रस्तावना

'Annona' हा शब्द लॅटिन वाक्प्रचारावरून (ज्याचा अर्थ 'वार्षिक कापणी' असा होतो) आला असून, या वनस्पतीचा समावेश 'Annonaceae' कुळात होतो. या कुळामध्ये सुमारे 2500 प्रजाती आणि 130 हून अधिक वंश (genera) आढळतात.

'Annona squamosa' (सीताफळ) या प्रजातीचा उगम 'नव्या जगातील' (New World) उष्णकटिबंधीय प्रदेशात झाला असावा असे मानले जाते; हीच प्रजाती सर्वाधिक मोठ्या प्रमाणावर लागवडीखाली असलेली विविधता आहे [1].

या लहान उष्णकटिबंधीय वृक्षाची लागवड सर्वप्रथम १९०८ मध्ये फ्लोरिडा येथे करण्यात आली आणि आता त्याचा प्रसार जगभर झाला आहे. आजपर्यंत, 'Annona' वंशातील पाच मुख्य प्रजातींची (A. squamosa, A. atemoya, A. cherimola, A. muricata आणि A. reticulata) जगभरात व्यावसायिक स्तरावर लागवड केली जात आहे. या फळाची विविध प्रादेशिक नावे पुढीलप्रमाणे आहेत: Custard Apple (CA), सीताफळ (भारत), Anon (पोर्तुगीज), Anona (इस्त्रायल/लेबनॉन), Shijia (चीनचा मुख्य भूभाग) आणि Pineapple Sugar Apple (तैवान, चीन) [2].

या फळामध्ये काही उत्कृष्ट गुणधर्म नैसर्गिकरित्याच आढळतात; उदा. बियांचे प्रमाण कमी असणे, काढणीनंतर दीर्घकाळ टिकून राहणे (साठवणूक करणे सोपे असणे) आणि फळाला तडे जाण्याचे प्रमाण अत्यंत कमी असणे. या गुणधर्मांमुळेच या फळाने जगभरात मोठ्या प्रमाणावर लक्ष वेधून घेतले आहे. सीताफळाचे जागतिक स्तरावरील प्रमुख उत्पादक प्रदेश 'आकृती १' मध्ये दर्शविले आहेत; यामध्ये भारत हा सीताफळाचा जगातील सर्वात मोठा उत्पादक देश आहे. NHB (राष्ट्रीय फलोत्पादन मंडळ, भारत) च्या अहवालानुसार, सध्या सुमारे ५५,००० हेक्टर क्षेत्र सीताफळाच्या लागवडीखाली आहे; तसेच, २०२३ मध्ये या फळाचे एकूण उत्पादन ३,८७,२६,००० टन इतके नोंदवले गेले आहे.  या फळाची निर्यात अंदाजे १,२०० टन इतकी झाली, ज्यातून १.०६ दशलक्ष डॉलर्सपेक्षा अधिक उत्पन्न मिळाले.

त्यापाठोपाठ तैवान (चीन) चा क्रमांक लागतो; येथे अंदाजे ५,५०० हेक्टर क्षेत्रावर 'सीए' (CA) फळाची लागवड केली जाते आणि त्यातून ६०३ दशलक्ष डॉलर्सचे उत्पादन मूल्य प्राप्त होते. 'Volza' च्या जागतिक निर्यात आकडेवारीनुसार, २०२३ मध्ये या फळाच्या निर्यातीत मागील वर्षाच्या तुलनेत ४५ टक्क्यांनी वाढ झाली असून, भारत, व्हिएतनाम आणि कोलंबिया हे प्रमुख निर्यातदार देश ठरले आहेत. आंतरराष्ट्रीय बाजारपेठेत या फळाचा सरासरी भाव ४ ते ६ डॉलर्स प्रति किलोग्राम इतका असतो; मात्र वाहतुकीचा खर्च अधिक असल्याने काही वेळा हा भाव १० डॉलर्सपर्यंतही पोहोचतो, ज्यामुळे 'सीए' हे एक उच्च-मूल्य असलेले फळ ठरते.

CA: कस्टर्ड ॲपल (सीताफळ)



Tuesday, March 17, 2026

Custard Apple (Annona squamosa)

 


. 2025 Oct 2;14(19):3413. doi: 10.3390/foods14193413

A Review of Nutrition, Bioactivities, and Health Benefits of Custard Apple (Annona squamosa): From Phytochemicals to Potential Application

Editors: Antonio CillaRafael Guillén Bejara

 Introduction

Annona, derived from the Latin phrase ‘annual harvest’, belongs to the family Annonaceae with about 2500 species and more than 130 genera. 

Annona squamosa, considered to have originated in the New World tropics, is the most widely cultivated variety []

. The small tropical tree was first bred in Florida in 1908, and now it has been spread worldwide. To date, five main varieties of Annona spp. (A. squamosaA. atemoyaA. cherimolaA. muricata, and A. reticulata) have been commercially cultivated in the world. Regional names of the fruit include the custard apple (CA), sitaphal (India), anon (Portuguese), anona (Israel/Lebanon), shijia (Chinese mainland), and pineapple sugar apple (Taiwan, China) [].

 It inherits fine qualities, such as having a small quantity of seeds, easy preservation after harvest, and rare cracking, garnering widespread attention. The major global producing regions are shown in Figure 1, and India is the largest producer of CA in the world. As reported by the NHB (National Horticulture Board, India), approximately 55,000 hectares are under CA cultivation, with production of the fruit reaching 38,726,000 tons in 2023; exports of the fruit were approximately 1200 tons, earning more than 1.06 million dollars.

 Taiwan, China follows with approximately 5500 hectares under CA cultivation and an output value of 603 million dollars. Volza’s Global Export Data shows that 2023 exports grew 45 percent year on year, with India, Vietnam, and Colombia as top exporters. The average international market price is between 4 and 6 dollars per kilogram, peaking at 10 dollars per  due to high transportation costs, making CA a high-value fruit.


CA cusstered  apple



Figure 1

Major global regions producing

Custard applies  




Saturday, March 14, 2026

Health benefits of Custard Apple ,Nutrtion Bioactivities

 

. 2025 Oct 2;14(19):3413. doi: 10.3390/foods14193413

A Review of Nutrition, Bioactivities, and Health Benefits of Custard Apple (Annona squamosa): From Phytochemicals to Potential Application

Editors: Antonio CillaRafael Guillén Bejara

Abstract

The custard apple (CA) is a noble fruit in tropical regions inworldwide. It has attracted a growing interest due to its organoleptic properties and nutritional value.

 With the expansion of international trade, both its cultivation and consumption have grown significantly in recent years. Previous researchers have sporadically investigated its nutritional composition and health benefits; however, existing information on its processing and utilization is highly fragmented and lacks a comprehensive overview of its constituents, biological activities, and potential applications. 

This review is a detailed summary of the nutritional and bioactive properties, safety evaluations, and potential applications of CA. Following PRISMA guidelines, peer-reviewed studies published between 2000 and 2025 were systematically searched in PubMed, Scopus, ResearchGate, and Web of Science. Inclusion criteria comprised studies reporting on nutritional composition, phytochemicals, bioactivities, health promotion, and applications of CA.

 In addition to primary nutrients like carbohydrates, protein, fatty acids, vitamins, and minerals, 

CA also contains a multitude of bioactive compounds, mainly including phenols, flavonoids, terpenoids, acetogenins, and alkaloids, which are attributed to a range of health benefits,

 such as antioxidant, anti-microbial, anti-tumor, blood sugar regulation, and cognitive function improvement.

 However, more clinical and toxicological profiles remain underexplored, and future research should focus on standardized extraction, safety evaluation, and translational applications. Additionally, the challenges and future perspectives in industrial applications are discussed, which are expected to offer comprehensive information for the utilization of CA.

Thesis References Path

  Thesis References Path 

1 Pub med
2Books
3 cross references 
4 Read the cross references care fully
With minimum time it's skill the title of reference will help you to
judge if it could help you.
5 keep a xcell record of each references how old is journal
When the first article was published.

6 pub med helps you to know eta when your reference was studied
Extensively
 Lastly write comments 
This is second article

How to write for Ph D thesis?

 How to write PhD Thesis?


Mostly student write  after completing research work.

This requires lot of time to finish writing 

The solution is 

Following tips

1 as soon as guide sends tile of thesis topic to University 

Start writing


2 Start writing Reviewof literature

As you know it is continuous process 


Library reading is required

Try to read full length article underline important lines key points.


3 This will save lot of time will help your presentation style

During conference.

4write material andmethods as you progress

5 Results description is on going process. Write

After experiment .

6 Discussion is most difficult chapter

Guide may not accept what you write as it is not result part

But the way your results different from previous what are new

findings.



Thursday, February 26, 2026

Crow is the Pilot





   Yes, the crow is a pilot, 

a passenger, a control tower


He does the work of the  control tower


No need for a black box, no petrol, but fuel is needed

Yesterday I. First the crow was eating a piece of bread and then

Pilot 


He planned where to fly


The food he eats is his food for his stomach and


And petrol is fuel.


How accurate is his vision? Flying in a moment


How difficult is life


How much energy does he get by eating?


How small is his brain but he has the strength to 

do the above tasks


Between a crow and a beggar, a crow is very good because he


Calls other friends with the food he gets

Wednesday, February 25, 2026

कावळा एक पायलट

 


              कावळा एक पायलट

हो कावळा एक पायलट आहेत प्रवासी आहे कंट्रोल

 टॉवर चे काम तोच करतो

ब्लॅक बॉक्स ची गरज नाही पेट्रोल नाही पण इंधन लागते

कालच मी. पहिले कावळा कुरमुरे  वेचुन  खात होता आणि नंतर 

 पायलट महाशय

उडाले कुठे जायचे ते  प्लान स्वतः कडे 

खाण्यात त्याच्या आलेले अन्न हेच त्याच्या पोटासाठी पोटपणी आणि 

आणि पेट्रोल समान इंधन.

किती अचूक दृष्टी धोके दिसता क्षणात उडणे 

खरच किती अवघड जीवन

किती खाऊन उडण्याची ऊर्जा येत असेल ?

मेंदू किती छोटा पण वरील कामे करण्यास ताकद असणारा

कावळा आणि भिकारी यात कावळा हा खूप चांगला कारण तो

मिळालेले खाद्य इतर दोस्तांना बोलावून देणारा



Saturday, February 14, 2026

इडली मार्केटिंग

 हो इडली मार्केटिंग केली जाते

काही वर्षे झाली अंदाजे  50 वर्षाहून अधिक काळ

मार्केटिंग स्टाईल आगळी वेगळी होती

कोणी इडली घेता का? आरोग्यास चांगली

अशा घोषणा नाहीत

रस्ताने हे विक्रेते फिरत पण तोंडाला आराम देऊन विक्री चांगली होत असे आज ही होते

काही एक रबराचा हॉर्न वाजवून तो ही हाताने तोंडाला आराम  ग्राहक बोलावी ते ठराविक आवाज आल्या. वर नवीन पोजिशन केली आज ही पध्दत आहे.

पाव  वाला पाव पाव आवाज देतो सायकल ने फिरतो

धार वाला धार् वाला म्हणतो

जूने समान वाला समान जून पुराणे घेतो असा आवाज देतो

आवाज ही गरज आहे ती बासरी विकणाऱ्याला  बासरी घेऊन

तीच बासरी ते गण आपण नाही गाऊ शकत




Tuesday, February 10, 2026

Effect of Air Pollution and Neurological Dsease


 


Ref

Front Public Health. 2022 Jul 14;10:882569. doi: 10.3389/fpubh.2022.882569

The Physiological Effects of Air Pollution: 

Particulate Matter,

 Physiology and Disease

Jack T Pryor 1,2, Lachlan O Cowley 1, Stephanie E Simonds 1,*


Abstract

Nine out of 10 people breathe air that does not meet World Health Organization pollution limits. 

Air pollutants include gasses and particulate matter and collectively are responsible for ~8 million annual deaths.

 Particulate matter is the most dangerous form of air pollution, 

causing inflammatory and oxidative tissue damage. 

A deeper understanding of the physiological effects of particulate matter is needed for effective disease prevention and treatment.

 This review will summarize the impact of particulate matter on physiological systems, and where possible will refer to apposite epidemiological and toxicological studies. By discussing a broad cross-section of available data, 

we hope this review appeals to a wide readership and provides some insight on the impacts of particulate matter on human health.


Particulate Matter

Particulate matter (PM) are solid compounds suspended in air that are sufficiently small to be inhaled (Figure 1)

. PM is categorized by particle diameter (measured in μm); PM0.1, PM2.5 and PM10 whilst 

ambient concentration is usually quantified as μg/m3.

 Some PM are of natural origin (bushfires, dust, sea spray, aerosols, etc.) but anthropogenic PM (diesel, coal and biomass combustion and emissions from metal refineries etc.) are the most dangerous to health (13).

 High atmospheric concentrations of human-made PM, and toxic and oxidative chemical characteristics render them disproportionately hazardous (13).

 Elemental and complex chemical species of PM are diverse, with surface shape, chemistry and charge impacted by emission source and environmental conditions. PM chemistry can change through reactions with other airborne PM and be affected by the oxidative effects of ozone and low ambient pH (14, 15).


Fig 1

To scale illustration of the relative sizes of PM10, PM2.5, and PM0.1. Representative macrophage and mitochondria are included to scale for

Reference






Fig1

Neurological Disease

Increased ambient PM concentration positively correlates with the incidence of Alzheimer's disease, Parkinson's disease, Multiple Sclerosis, dementia and autism spectrum disorder (Figure 2) (127)

. Long-term PM2.5 exposure significantly increased age adjusted risk of mortality and hospital admission for Alzheimer's disease, Parkinson's disease and non-Alzheimer's disease dementia (128). 

This study found the strongest correlation to exist between PM2.5 and Alzheimer's disease (128). One longitudinal study found that people living within 50 meters of a main road had a 12% greater chance of dementia diagnosis (129).

 PM2.5 exposure is linked to faster decline in new learning and immediate recall, as well as MRI-detected gray matter atrophy in brain areas vulnerable to Alzheimer's disease pathology (130).

 PM2.5 exposure has been linked to Alzheimer's specific cognitive impairments (CERAD score but not ABC score) however post-mortem analysis of neuropathology in the brains of Alzheimer's disease patients failed to reveal any link between PM2.5 exposure 10 years before death, and disease progression indicated by Braak stage (131)

. The impact of specific PM (including black carbon, organic matter, nitrate, sulfate, sea salt and soil) exposure on the rate of initial Parkinson's disease hospitalization in New York State was investigated. This study revealed that with each standard deviation increase in either nitrate or organic matter PM, the risk of hospitalizations increased 1.06-fold (132).


PM 0.1 can cross the blood brain barrier and cause inflammatory and oxidative tissue damage as well as microglial activation (133). 

Glutamatergic excitotoxicity is a common reported endpoint for acute PM induced pathophysiology in the central nervous system. PM has been found in neurons, glia, endothelium, choroid plexus ependymal cells, cerebrospinal fluid, nasal epithelium, and olfactory epithelium of individuals subjected to PM exposure (134).

 PM2.5 has been found to reduce nervous system expression of the tight junction proteins, zonula occludens 1 and 2 (135). 

This study found a compromised blood brain barrier permeable to macrophage infiltration, and nervous system tissue subject to glutamatergic excitotoxicity, triggered by macrophage-derived glutamate (135).

 In mice, PM2.5 has been shown to reach the olfactory bulb and induce microglial activation and glutamatergic excitotoxicity that could be blocked with the antioxidant N-acetylcysteine (136).


Alzheimer's disease is characterized by cortical and hippocampal amyloid-β plaque and tau tangle deposition. Amyloid-β plaque formation and gliosis underlie at least some of the cognitive deficits associated with 

AD progression (137).

 In a transgenic mouse model of Alzheimer's disease, exposure to diesel emission PM2.5 exacerbated amyloid-β plaque deposition, and increased astrocytosis and microgliosis. Additionally, elevated inflammatory cytokines including tumor necrosis factor, nuclear factor-α, interleukins 1β and 6, interferon-γ and macrophage inflammatory protein-3α were identified in the cortices of double transgenic mice (138).

 In a similar study, 13-week exposure to diesel exhaust PM also accelerated cortical amyloid-β plaque deposition, an effect associated with significant impairments to motor coordination (139). Parkinson's disease is caused by loss of dopaminergic neurons in the substantia nigra of the basal ganglia. Neuron loss results in diminished cortical input and associated behavioral and cognitive deficits. In a rotenone-induced mouse model of Parkinson's disease, PM2.5 exposure induced mitochondrial dysfunction, oxidative stress and apoptosis in the substantia nigra. In the same study, PM exposure also exacerbated motor and somatosensory deficits (140). 

Multiple Sclerosis (MS) is a progressive, demyelinating and neurodegenerative disease of the CNS. Short-term PM exposure is associated with increased MS hospital admissions and relapse (127). In a mouse model of lipophosphatidylcholine-induced demyelination, PM exposure impairs myelin repair and sustains astroglia and microglia dependent neuroinflammation. PM2.5 exposure to rats impaired spatial learning and memory, inquiring ability and sensory function, these changes were related to ultrastructural changes to mitochondria and myelin (141).

 Mice exposed to PM2.5 for 10 months developed structural hippocampal alterations including diminished apical spine density and dendritic branching of hippocampal neurons and behavioral studies revealed reduced spatial learning and memory impairments (142).

Sunday, February 8, 2026

Effects of Air Pollution and Endocrine Disease

 


Ref

Front Public Health. 2022 Jul 14;10:882569. doi: 10.3389/fpubh.2022.882569

The Physiological Effects of Air Pollution: Particulate Matter, Physiology and Disease

Jack T Pryor 1,2, Lachlan O Cowley 1, Stephanie E Simonds 1,*

Endocrine Disease

The known effects of cigarette smoke on reproductive and thyroid hormones provide indications of the risks associated with PM exposure.

 Cigarette smoke is a risk factor in Graves hypothyroidism and is associated with elevated plasma cortisol, aldosterone, adrenal androgens and impacts female fertility by increasing steroid hormone binding globulin and decreasing circulating free estrogens (83–86). 

Several PM species have been identified as endocrine disrupting chemicals (87).

 In humans PM exposure is linked to insulin resistance, elevated circulating adipokines, hypothyroidism and (mixed) estrogenic effects (88). 

Thyroid hormones triiodothyronine (T3) and thyroxine (T4) regulate metabolic rate, cardiovascular tone and promote growth rate during fetal development and early life (89).

 In humans, PM exposure is associated with decreased plasma T4 both in pregnant women and new-borns, as well as congenital hypothyroidism and reduced infant birth weight (90). 

Black carbon, ammonia, organic matter and nitrate PM species appear to have the strongest links to thyroid dysfunction (91–94). 

Effective insulin signaling is required for glucose homeostasis, and insulin resistance is closely associated with obesity and is a risk factor for the onset of type-2 diabetes (95).

 PM exposure is associated with insulin resistance and non-alcoholic fatty liver disease, driven by oxidative stress and dyslipidaemia (96, 97).

 Together these studies highlight the link between air pollution and metabolic diseases including diabetes. Of >106 chemicals to which gas and oil extraction workers are exposed, 21 have been shown to exert estrogenic, androgenic and/or steroidogenic effects (98).

 Some chemicals identified as impacting endocrine function include benzene, toluene, ethylbenzene xylene, mercury, polychlorinated dibenzodioxins (PBDDs) and several polycyclic aromatic hydrocarbons (PAH) (88, 98, 99).

 Atmospheric sources of PAHs are vehicle emissions and biomass and coal combustion. Low molecular weight PAHs are in gas phase whereas high molecular weight PAHs are bound to the surface of PM (100). PAHs are classed as endocrine disrupting compounds and have been found to both increase and decrease estrogen receptor mRNA expression and function (REF). Estrogenic dysfunction has been shown to be both direct at estrogen receptors and indirect via aryl hydrocarbon receptor (AhR) signaling (101, 102). 

PBDDs also exert endocrine effects via AhRs, and preclinical experiments have shown AhR-mediated effects of dioxin exposure to include weight loss, reproductive and developmental toxicity, tumorigenesis and immune system dysfunction (103). 

PM contains many metal elements, some of which interfere with estrogenic signaling by mimicking endogenous estrogens (104). Metalloestrogens include aluminum, selenium, antimony, arsenic (arsenite; NaAsO2), barium, cadmium, chromium, cobalt, copper, lead, mercury, nickel, tin and vanadium (vanadate; V2O5) (16, 104).


Obesity and Diabetes

In humans, the association between PM2.5 exposure and obesity is dependent on age, gender and socioeconomic demographic (105, 106).

 A growing body of evidence indicates that PM2.5 exposure is a risk factor for reduced skeletal muscle mass, obesity, diabetes and hypertension (107–109). 

Long-term PM exposure is associated with a high risk for type 2 diabetes, and road traffic-specific PM is correlated with an elevated risk (110). 

Increased incidence of type-2 diabetes remains when adjusted for age, body mass index (BMI), and socioeconomic status (111, 112). 

PM exposure is associated with higher levels of circulating complement factor 3 (C3c), and women with elevated plasma C3c are more susceptible to diabetes than those with low C3c (112). PM2.5 exposure is associated with a faster decline in insulin sensitivity during childhood and higher BMI by age 18 (113–115). 

The associated between PM exposure and hypertension is greater in overweight and obese children (116). In animal studies, exposure of rats to PM increased chocolate consumption whereas in chow-fed wild-type mice, 10-week PM2.5 exposure increased visceral fat mass, insulin resistance and adipose tissue inflammation (117, 118). In mice, short-term PM exposure increased food intake, fat mass and UCP-1 expression in brown adipose tissue (119). PM exposure also induced hypothalamic inflammation indicated by increased microglia density, increased toll-like receptor-4 and elevated inhibitory nuclear factor-kappa-B-kinase-epsilon expression (119). After 12 weeks of PM exposure, mice exhibited increased food intake and elevated fat mass and had lower energy expenditure. Mice had elevated levels of plasma leptin and insulin and increased Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) indicators of insulin resistance (119). This same study also revealed that PM exposure decreased hypothalamic satiety markers, including reduced levels of phosphorylated STAT 3, and diminished proopiomelanocortin expression (119).


PM exposure to mice was found to induce hepatic oxidative stress, inflammation, negatively affect glucose tolerance and induce insulin resistance (96, 120). Interestingly PM exposure has been found to increase hepatic triacylglycerols, free fatty acids and cholesterol levels in female but not in male mice (96). In addition to insulin resistance, PM exposure has been shown to exert toxic effects directly on the pancreas (121). In a streptozotocin-induced mouse model of type-1 diabetes, PM from diesel exhaust fumes exacerbated pancreatic cell vacuolation and islet cell apoptosis, increased pancreatic amylase activity, increased expression of oxidative stress markers 8-isoprostane and superoxide dismutase and reduced levels of the antioxidant glutathione peroxidase (121). In a rat model of gestational diabetes PM exposure induced maternal pancreatic inflammation indicated by diminished pancreatic glucose transporter-2 expression (122).